RECENT ADVANCES IN ALZHEIMER'S RESEARCH

[Guest guest]

Alois Alzheimer was born on 14th of June 1864

in Marktbreit am Main (Germany) and died in Breslau (now Wroclaw, Poland) on

December 19, 1915. Alzheimer’s most widely known contribution to the

Neurosciences is the histological description of the disease that was named latterly after

him by Emil Kraepelin. It was in Kraepelin’s clinic in Munich where Alzheimer’s life as a scientist came to full fruition. Following is the primary source reference:Kraepelin E (1910). Psychiatrie. Ein Lehrbuch für Studierende

und Ärzte. II. Band, Klinische Psychiatrie. Verlag Johann Ambrosius Barth, Leipzig.-----Syed Ziaur Rahman, MDSchool of MedicineUniversity of Western Sydney

AustraliaOn Mon, Sep 12, 2011 at 12:30 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

A very good morning to all NETRUMIANS. I am Mrinmoy Chakrabarty, from Dept. of Pharmacology, Veer Chandra Singh Garhwali Govt. Medical College and Research Institute, Srinagar, Pauri Garhwal, Uttarakhand. I am commencing a discussion on " RECENT ADVANCES IN ALZHEIMER'S RESEARCH " today and look forward to interacting with you on this theme. I expect to be able to cast light/ views on some of your queries or opinions and at the same time get stumped by the sheer insight of others. But then, that is the factor that spurs us to e- network for discussion on a topic. I felt a better discussion on the main theme would be facilitated with some information on few topics surrounding it and hence, am taking it up in a step wise manner with appropriate peripheral content.

1. Premise

Decades of research have proved futile to rein in the relentless progression of Alzheimer's disease (AD). With some of the most promising forerunner therapeutic molecules failing in late phase clinical trials lately and the existing modern therapies yielding only modest, short term benefits at the cost of different side effects, the scenario as of now is grim and looms large with the world burden of Alzheimer's slated to touch 65.7 million  mark by 2030 and 115.4 million by 2050.

The disease biology is still obscure with experts trying to have a better handle on the course of the disease progression. Every small detail is being re read, every single hypothesis scrutinized and every single notion re- considered to put together the pieces of the Alzheimer's puzzle.

 

2. A Brief History

AD was discovered in 1907 by Alois Alzheimer, but was not considered a major disease or disorder until the 1970s. Alzheimer documented a case of a woman in her fifties, August Deter who exhibited severe cognitive disorders pertaining to memory, language, and social interaction, according to Khachaturian and Radebaugh who have authored a book titled   " Alzheimer's disease: Cause(s), Diagnosis, Treatment, and Care. "

After the patient's death, Alzheimer performed an autopsy on her brain, using a silver staining technique that allowed him to visualize the neurons. In the process he found unusual formations, now known as amyloid plaques and neurofibrillary tangles. Alzheimer hypothesized that these lesions might be the cause or effect of the as yet to be named AD, or possibly a combination of the two. The disorder was later named after Alzheimer as more people were found to have the symptoms associated with his findings. 

In retrospect, before Alzheimer's 1907 discovery, scientists, clinicians and laymen took dementia as a " natural " progression of age, and " senility was accepted as a part of aging. "

Additionally, AD was not differentiated from other types of age-induced dementia or senility. AD did not suddenly " appear " in 1907, rather it was then that the disease was first recognized and named.

Even with Alzheimer's discovery, however, the disease was not one that was accepted as, well, a " disease. " Senility and dementia were still considered part of the aging process. Whaley states that AD did not become a common term, or even a large concern, until neurobiological research exploded in the late 1970s.

 

3. Dementia:

With a greater degree of prosperity setting in, we have a bigger ageing population to deal with and increasing age goes hand in hand with many of its attendant risks.

Dementia is one such prominent one for which we do not have a prevention, leave alone cure. It is defined as a generalized loss of cognitive abilities, including impairment of learning-memory with one or more of aphasia (defect or loss of power of expression by speech, writing, signs), apraxia (loss of ability to carry out familiar, purposeful movements, esp. inability to use objects correctly), agnosia (inability to recognize the import of sensory impressions e.g. auditory, gustatory, olfactory, tactile, visual), disturbed planning, organizing, abstract thinking abilities.

To simplify it is the loss of thinking, memory, and reasoning — that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that might accompany certain diseases or conditions. Symptoms also might include changes in personality, mood, and behaviour. Dementia is irreversible when caused by disease or injury, but might be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression.

Dementia develops when the parts of the brain that are involved with learning, memory, decision-making, and language are affected by any of various infections or diseases. The most common cause of dementia is AD, but there are as many as 50 other known causes.

Some of the disorders that cause dementia might be reversible, although unfortunately most types of dementia do not respond to treatment.

 

There are many causes of dementia but the most common causes include:

Degenerative neurological diseases, such as Alzheimer's, dementia with Lewy bodies, Parkinson's, and Huntington's

Vascular disorders, such as multiple-infarct dementia, which is causes by multiple strokes in the brain

Infections that affect the central nervous system, such as HIV dementia complex and Creutzfeldt-Jakob disease

Chronic drug use

Depression

Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from developmental abnormalities, infections, injury, or brain tumors

AD causes 50 percent to 70 percent of all dementia. However, researchers are finding that some of what was previously considered AD is really one of two other degenerative diseases: Lewy body disease and Pick's disease. There also are a number of other important disorders that can lead to dementia.

Dementia is considered a late-life disease because it tends to develop mostly in elderly people. About 5 percent to 8 percent of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. It is estimated that as many as half of people 85 or older suffer from dementia.

Dementia is not a disease; it is the clinical presentation or symptoms of a disease. In a nutshell, dementia is a symptom, and AD is the cause of the symptom.

4. Types of dementia

Although they are classified variedly based on different criteria, one of the broadest classifications based on the part of brain that is principally affected is

Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layers of the brain that play a critical role in cognitive processes such as learning,   memory and language. Alzheimer's and Creutzfeldt-Jakob disease are two forms of cortical dementia. Cortical dementia typically show severe memory impairment and aphasia.

 

Subcortical dementias result from dysfunction in the parts of the brain that are beneath the cortex. Usually, the memory loss and language difficulties that are characteristic of cortical dementias are not seen. Rather, people with subcortical dementias, such as Huntington's disease, Parkinson's Disease, and AIDS dementia complex, tend to show changes in their personality and attention span, stagnancy and slowing in thinking.

 

Treatable causes of dementia are reversible disorders that can be cured completely, or at least partially, by treating the underlying disorder. For example, dementia caused by any of the following are often at least partially treatable:

Chronic drug abuse

Tumours that can be removed

Subdural hematoma, an accumulation of blood beneath the outer covering of the brain that results from a broken blood vessel, usually as a result of a head injury (which can be minor and even unrecognized)

Normal pressure hydrocephalus

Metabolic disorders, such as a vitamin B12 deficiency

Hypothyroidism, a condition that results from low levels of thyroid secretion

Hypoglycemia, a condition that results from low blood sugar

Non-treatable causes of dementia include:

AD

Multi-infarct dementia

Dementias associated with Parkinson's disease and similar disorders

AIDS dementia complex

Creutzfeldt-Jakob disease (CJD), a quickly progressing and fatal disease that is characterized by dementia and myoclonus — muscle twitching and spasm

Since it is Day 1 of the discussion, we restrict ourselves to these generalized aspects and gradually move to the thick of Alzheimer's neurodegeneration in the days to come. Looking forward to your participation and Have A Great Day Ahead .

 

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

More clear version on historical aspect:

In 1907, Alzheimer published his now famous report on a 51- year-old

woman who had come under his care in 1901 while he worked as an attending

physician in the furt Asylum. The original case file of this patient,

Auguste D., was discovered recently, and it has been speculated that the

patient’s dementia was not caused by the typical neurodegeneration of Alzheimer

disease but by arteriosclerosis of the brain. Alzheimer’s report on Auguste D.

is not a full-size research paper but an abstract summarizing the presentation

he gave at the 37th Meeting of the Southwest German Psychiatrists in

Tubingen on November 3, 1906. Therefore, the first report by Alzheimer on the

morphology of the disease that was named after him by Emil Kraepelin in 1910 does

not contain any illustrations. Yet numerous figures, mainly drawings, which

include several examples of the histopathology of his first case were published

by Alzheimer in 1911 together with a second case report (Zbl. ges. Neurol.

Psych. 4: 356–385). In the report on his second published case, Alzheimer gives

a detailed description of the clinical history of a 56-year-old (Johann F.) who

suffered from presenile dementia and who was hospitalized in Kraepelin’s clinic

for more than 3 years. According to Alzheimer’s notes the patient was admitted

to the psychiatric clinic on November 12, 1907.

-------------------On Mon, Sep 12, 2011 at 1:13 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

Alois Alzheimer was born on 14th of June 1864

in Marktbreit am Main (Germany) and died in Breslau (now Wroclaw, Poland) on

December 19, 1915. Alzheimer’s most widely known contribution to the

Neurosciences is the histological description of the disease that was named latterly after

him by Emil Kraepelin. It was in Kraepelin’s clinic in Munich where Alzheimer’s life as a scientist came to full fruition. Following is the primary source reference:Kraepelin E (1910). Psychiatrie. Ein Lehrbuch für Studierende

und Ärzte. II. Band, Klinische Psychiatrie. Verlag Johann Ambrosius Barth, Leipzig.-----Syed Ziaur Rahman, MDSchool of MedicineUniversity of Western Sydney

AustraliaOn Mon, Sep 12, 2011 at 12:30 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

A very good morning to all NETRUMIANS. I am Mrinmoy Chakrabarty, from Dept. of Pharmacology, Veer Chandra Singh Garhwali Govt. Medical College and Research Institute, Srinagar, Pauri Garhwal, Uttarakhand. I am commencing a discussion on " RECENT ADVANCES IN ALZHEIMER'S RESEARCH " today and look forward to interacting with you on this theme. I expect to be able to cast light/ views on some of your queries or opinions and at the same time get stumped by the sheer insight of others. But then, that is the factor that spurs us to e- network for discussion on a topic. I felt a better discussion on the main theme would be facilitated with some information on few topics surrounding it and hence, am taking it up in a step wise manner with appropriate peripheral content.

1. Premise

Decades of research have proved futile to rein in the relentless progression of Alzheimer's disease (AD). With some of the most promising forerunner therapeutic molecules failing in late phase clinical trials lately and the existing modern therapies yielding only modest, short term benefits at the cost of different side effects, the scenario as of now is grim and looms large with the world burden of Alzheimer's slated to touch 65.7 million  mark by 2030 and 115.4 million by 2050.

The disease biology is still obscure with experts trying to have a better handle on the course of the disease progression. Every small detail is being re read, every single hypothesis scrutinized and every single notion re- considered to put together the pieces of the Alzheimer's puzzle.

 

2. A Brief History

AD was discovered in 1907 by Alois Alzheimer, but was not considered a major disease or disorder until the 1970s. Alzheimer documented a case of a woman in her fifties, August Deter who exhibited severe cognitive disorders pertaining to memory, language, and social interaction, according to Khachaturian and Radebaugh who have authored a book titled   " Alzheimer's disease: Cause(s), Diagnosis, Treatment, and Care. "

After the patient's death, Alzheimer performed an autopsy on her brain, using a silver staining technique that allowed him to visualize the neurons. In the process he found unusual formations, now known as amyloid plaques and neurofibrillary tangles. Alzheimer hypothesized that these lesions might be the cause or effect of the as yet to be named AD, or possibly a combination of the two. The disorder was later named after Alzheimer as more people were found to have the symptoms associated with his findings. 

In retrospect, before Alzheimer's 1907 discovery, scientists, clinicians and laymen took dementia as a " natural " progression of age, and " senility was accepted as a part of aging. "

Additionally, AD was not differentiated from other types of age-induced dementia or senility. AD did not suddenly " appear " in 1907, rather it was then that the disease was first recognized and named.

Even with Alzheimer's discovery, however, the disease was not one that was accepted as, well, a " disease. " Senility and dementia were still considered part of the aging process. Whaley states that AD did not become a common term, or even a large concern, until neurobiological research exploded in the late 1970s.

 

3. Dementia:

With a greater degree of prosperity setting in, we have a bigger ageing population to deal with and increasing age goes hand in hand with many of its attendant risks.

Dementia is one such prominent one for which we do not have a prevention, leave alone cure. It is defined as a generalized loss of cognitive abilities, including impairment of learning-memory with one or more of aphasia (defect or loss of power of expression by speech, writing, signs), apraxia (loss of ability to carry out familiar, purposeful movements, esp. inability to use objects correctly), agnosia (inability to recognize the import of sensory impressions e.g. auditory, gustatory, olfactory, tactile, visual), disturbed planning, organizing, abstract thinking abilities.

To simplify it is the loss of thinking, memory, and reasoning — that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that might accompany certain diseases or conditions. Symptoms also might include changes in personality, mood, and behaviour. Dementia is irreversible when caused by disease or injury, but might be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression.

Dementia develops when the parts of the brain that are involved with learning, memory, decision-making, and language are affected by any of various infections or diseases. The most common cause of dementia is AD, but there are as many as 50 other known causes.

Some of the disorders that cause dementia might be reversible, although unfortunately most types of dementia do not respond to treatment.

 

There are many causes of dementia but the most common causes include:

Degenerative neurological diseases, such as Alzheimer's, dementia with Lewy bodies, Parkinson's, and Huntington's

Vascular disorders, such as multiple-infarct dementia, which is causes by multiple strokes in the brain

Infections that affect the central nervous system, such as HIV dementia complex and Creutzfeldt-Jakob disease

Chronic drug use

Depression

Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from developmental abnormalities, infections, injury, or brain tumors

AD causes 50 percent to 70 percent of all dementia. However, researchers are finding that some of what was previously considered AD is really one of two other degenerative diseases: Lewy body disease and Pick's disease. There also are a number of other important disorders that can lead to dementia.

Dementia is considered a late-life disease because it tends to develop mostly in elderly people. About 5 percent to 8 percent of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. It is estimated that as many as half of people 85 or older suffer from dementia.

Dementia is not a disease; it is the clinical presentation or symptoms of a disease. In a nutshell, dementia is a symptom, and AD is the cause of the symptom.

4. Types of dementia

Although they are classified variedly based on different criteria, one of the broadest classifications based on the part of brain that is principally affected is

Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layers of the brain that play a critical role in cognitive processes such as learning,   memory and language. Alzheimer's and Creutzfeldt-Jakob disease are two forms of cortical dementia. Cortical dementia typically show severe memory impairment and aphasia.

 

Subcortical dementias result from dysfunction in the parts of the brain that are beneath the cortex. Usually, the memory loss and language difficulties that are characteristic of cortical dementias are not seen. Rather, people with subcortical dementias, such as Huntington's disease, Parkinson's Disease, and AIDS dementia complex, tend to show changes in their personality and attention span, stagnancy and slowing in thinking.

 

Treatable causes of dementia are reversible disorders that can be cured completely, or at least partially, by treating the underlying disorder. For example, dementia caused by any of the following are often at least partially treatable:

Chronic drug abuse

Tumours that can be removed

Subdural hematoma, an accumulation of blood beneath the outer covering of the brain that results from a broken blood vessel, usually as a result of a head injury (which can be minor and even unrecognized)

Normal pressure hydrocephalus

Metabolic disorders, such as a vitamin B12 deficiency

Hypothyroidism, a condition that results from low levels of thyroid secretion

Hypoglycemia, a condition that results from low blood sugar

Non-treatable causes of dementia include:

AD

Multi-infarct dementia

Dementias associated with Parkinson's disease and similar disorders

AIDS dementia complex

Creutzfeldt-Jakob disease (CJD), a quickly progressing and fatal disease that is characterized by dementia and myoclonus — muscle twitching and spasm

Since it is Day 1 of the discussion, we restrict ourselves to these generalized aspects and gradually move to the thick of Alzheimer's neurodegeneration in the days to come. Looking forward to your participation and Have A Great Day Ahead .

 

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

Following is a case history of Johann F, who was admitted to the

psychiatric clinic on November 12, 1907.

 

According to Alois Alzheimer, there was no history of excessive drinking.

In the previous 6 months he had become forgetful, could not find his way, could

not perform simple tasks or carried these out with difficulty. He stood around,

did not bother about food, but ate greedily whatever was put in front of him.

He was not capable of buying anything for himself and did not wash. He was

admitted by the service for the poor. After 3 years of hospitalization and

repeated clinical examinations, Johann F. died on October 3, 1910, in the Royal

Psychiatric Clinic in Munich showing features of pneumonia. Neuropathological examination

of his brain revealed the wide-spread presence of amyloid plaques but not a

single neuron showing neurofibrillary change.

 

Alzheimer provides ample clinical, biographic and neuropathological

data of this patient which have allowed present scientists to identify

histological sections found among archival material at the Institute of

Neuropathology of the University of Munich. Using recently established methods for

the molecular genetic analysis of neuropathological tissue, it has been able to

perform mutational screening of exon 17 of the amyloid precursor protein (APP)

gene and genotyping for apolipoprotein E (APOE) alleles.

 

The history of this discovery in detail could be found at: M. B.

Graeber, S. Kosel, R. Egensperger, R. B. Banati, U. Muller, K. Bise, P. Hoff, H.

J. Moller, K. Fujisawa and P. Mehraein. Rediscovery of the case described by

Alois Alzheimer in 1911: historical, histological and molecular genetic analysis.

Neurogenetics 1997; 1 (1): 73–80.

On Mon, Sep 12, 2011 at 1:34 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

More clear version on historical aspect:

In 1907, Alzheimer published his now famous report on a 51- year-old

woman who had come under his care in 1901 while he worked as an attending

physician in the furt Asylum. The original case file of this patient,

Auguste D., was discovered recently, and it has been speculated that the

patient’s dementia was not caused by the typical neurodegeneration of Alzheimer

disease but by arteriosclerosis of the brain. Alzheimer’s report on Auguste D.

is not a full-size research paper but an abstract summarizing the presentation

he gave at the 37th Meeting of the Southwest German Psychiatrists in

Tubingen on November 3, 1906. Therefore, the first report by Alzheimer on the

morphology of the disease that was named after him by Emil Kraepelin in 1910 does

not contain any illustrations. Yet numerous figures, mainly drawings, which

include several examples of the histopathology of his first case were published

by Alzheimer in 1911 together with a second case report (Zbl. ges. Neurol.

Psych. 4: 356–385). In the report on his second published case, Alzheimer gives

a detailed description of the clinical history of a 56-year-old (Johann F.) who

suffered from presenile dementia and who was hospitalized in Kraepelin’s clinic

for more than 3 years. According to Alzheimer’s notes the patient was admitted

to the psychiatric clinic on November 12, 1907.

-------------------On Mon, Sep 12, 2011 at 1:13 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

Alois Alzheimer was born on 14th of June 1864

in Marktbreit am Main (Germany) and died in Breslau (now Wroclaw, Poland) on

December 19, 1915. Alzheimer’s most widely known contribution to the

Neurosciences is the histological description of the disease that was named latterly after

him by Emil Kraepelin. It was in Kraepelin’s clinic in Munich where Alzheimer’s life as a scientist came to full fruition. Following is the primary source reference:Kraepelin E (1910). Psychiatrie. Ein Lehrbuch für Studierende

und Ärzte. II. Band, Klinische Psychiatrie. Verlag Johann Ambrosius Barth, Leipzig.-----Syed Ziaur Rahman, MDSchool of MedicineUniversity of Western Sydney

AustraliaOn Mon, Sep 12, 2011 at 12:30 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

A very good morning to all NETRUMIANS. I am Mrinmoy Chakrabarty, from Dept. of Pharmacology, Veer Chandra Singh Garhwali Govt. Medical College and Research Institute, Srinagar, Pauri Garhwal, Uttarakhand. I am commencing a discussion on " RECENT ADVANCES IN ALZHEIMER'S RESEARCH " today and look forward to interacting with you on this theme. I expect to be able to cast light/ views on some of your queries or opinions and at the same time get stumped by the sheer insight of others. But then, that is the factor that spurs us to e- network for discussion on a topic. I felt a better discussion on the main theme would be facilitated with some information on few topics surrounding it and hence, am taking it up in a step wise manner with appropriate peripheral content.

1. Premise

Decades of research have proved futile to rein in the relentless progression of Alzheimer's disease (AD). With some of the most promising forerunner therapeutic molecules failing in late phase clinical trials lately and the existing modern therapies yielding only modest, short term benefits at the cost of different side effects, the scenario as of now is grim and looms large with the world burden of Alzheimer's slated to touch 65.7 million  mark by 2030 and 115.4 million by 2050.

The disease biology is still obscure with experts trying to have a better handle on the course of the disease progression. Every small detail is being re read, every single hypothesis scrutinized and every single notion re- considered to put together the pieces of the Alzheimer's puzzle.

 

2. A Brief History

AD was discovered in 1907 by Alois Alzheimer, but was not considered a major disease or disorder until the 1970s. Alzheimer documented a case of a woman in her fifties, August Deter who exhibited severe cognitive disorders pertaining to memory, language, and social interaction, according to Khachaturian and Radebaugh who have authored a book titled   " Alzheimer's disease: Cause(s), Diagnosis, Treatment, and Care. "

After the patient's death, Alzheimer performed an autopsy on her brain, using a silver staining technique that allowed him to visualize the neurons. In the process he found unusual formations, now known as amyloid plaques and neurofibrillary tangles. Alzheimer hypothesized that these lesions might be the cause or effect of the as yet to be named AD, or possibly a combination of the two. The disorder was later named after Alzheimer as more people were found to have the symptoms associated with his findings. 

In retrospect, before Alzheimer's 1907 discovery, scientists, clinicians and laymen took dementia as a " natural " progression of age, and " senility was accepted as a part of aging. "

Additionally, AD was not differentiated from other types of age-induced dementia or senility. AD did not suddenly " appear " in 1907, rather it was then that the disease was first recognized and named.

Even with Alzheimer's discovery, however, the disease was not one that was accepted as, well, a " disease. " Senility and dementia were still considered part of the aging process. Whaley states that AD did not become a common term, or even a large concern, until neurobiological research exploded in the late 1970s.

 

3. Dementia:

With a greater degree of prosperity setting in, we have a bigger ageing population to deal with and increasing age goes hand in hand with many of its attendant risks.

Dementia is one such prominent one for which we do not have a prevention, leave alone cure. It is defined as a generalized loss of cognitive abilities, including impairment of learning-memory with one or more of aphasia (defect or loss of power of expression by speech, writing, signs), apraxia (loss of ability to carry out familiar, purposeful movements, esp. inability to use objects correctly), agnosia (inability to recognize the import of sensory impressions e.g. auditory, gustatory, olfactory, tactile, visual), disturbed planning, organizing, abstract thinking abilities.

To simplify it is the loss of thinking, memory, and reasoning — that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that might accompany certain diseases or conditions. Symptoms also might include changes in personality, mood, and behaviour. Dementia is irreversible when caused by disease or injury, but might be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression.

Dementia develops when the parts of the brain that are involved with learning, memory, decision-making, and language are affected by any of various infections or diseases. The most common cause of dementia is AD, but there are as many as 50 other known causes.

Some of the disorders that cause dementia might be reversible, although unfortunately most types of dementia do not respond to treatment.

 

There are many causes of dementia but the most common causes include:

Degenerative neurological diseases, such as Alzheimer's, dementia with Lewy bodies, Parkinson's, and Huntington's

Vascular disorders, such as multiple-infarct dementia, which is causes by multiple strokes in the brain

Infections that affect the central nervous system, such as HIV dementia complex and Creutzfeldt-Jakob disease

Chronic drug use

Depression

Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from developmental abnormalities, infections, injury, or brain tumors

AD causes 50 percent to 70 percent of all dementia. However, researchers are finding that some of what was previously considered AD is really one of two other degenerative diseases: Lewy body disease and Pick's disease. There also are a number of other important disorders that can lead to dementia.

Dementia is considered a late-life disease because it tends to develop mostly in elderly people. About 5 percent to 8 percent of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. It is estimated that as many as half of people 85 or older suffer from dementia.

Dementia is not a disease; it is the clinical presentation or symptoms of a disease. In a nutshell, dementia is a symptom, and AD is the cause of the symptom.

4. Types of dementia

Although they are classified variedly based on different criteria, one of the broadest classifications based on the part of brain that is principally affected is

Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layers of the brain that play a critical role in cognitive processes such as learning,   memory and language. Alzheimer's and Creutzfeldt-Jakob disease are two forms of cortical dementia. Cortical dementia typically show severe memory impairment and aphasia.

 

Subcortical dementias result from dysfunction in the parts of the brain that are beneath the cortex. Usually, the memory loss and language difficulties that are characteristic of cortical dementias are not seen. Rather, people with subcortical dementias, such as Huntington's disease, Parkinson's Disease, and AIDS dementia complex, tend to show changes in their personality and attention span, stagnancy and slowing in thinking.

 

Treatable causes of dementia are reversible disorders that can be cured completely, or at least partially, by treating the underlying disorder. For example, dementia caused by any of the following are often at least partially treatable:

Chronic drug abuse

Tumours that can be removed

Subdural hematoma, an accumulation of blood beneath the outer covering of the brain that results from a broken blood vessel, usually as a result of a head injury (which can be minor and even unrecognized)

Normal pressure hydrocephalus

Metabolic disorders, such as a vitamin B12 deficiency

Hypothyroidism, a condition that results from low levels of thyroid secretion

Hypoglycemia, a condition that results from low blood sugar

Non-treatable causes of dementia include:

AD

Multi-infarct dementia

Dementias associated with Parkinson's disease and similar disorders

AIDS dementia complex

Creutzfeldt-Jakob disease (CJD), a quickly progressing and fatal disease that is characterized by dementia and myoclonus — muscle twitching and spasm

Since it is Day 1 of the discussion, we restrict ourselves to these generalized aspects and gradually move to the thick of Alzheimer's neurodegeneration in the days to come. Looking forward to your participation and Have A Great Day Ahead .

 

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

Thanks Dr Rahman and Dr Chakrabarty for this excellent discussion. Would be great to have Dr Chakrabarty also quoting the references in his write ups as exemplified by Dr Rahman's posts. Apologies for pointing this out as an oversight in case it is being actually done already.

warm regards,rakeshOn Mon, Sep 12, 2011 at 9:21 AM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

 

Following is a case history of Johann F, who was admitted to the

psychiatric clinic on November 12, 1907.

 

According to Alois Alzheimer, there was no history of excessive drinking.

In the previous 6 months he had become forgetful, could not find his way, could

not perform simple tasks or carried these out with difficulty. He stood around,

did not bother about food, but ate greedily whatever was put in front of him.

He was not capable of buying anything for himself and did not wash. He was

admitted by the service for the poor. After 3 years of hospitalization and

repeated clinical examinations, Johann F. died on October 3, 1910, in the Royal

Psychiatric Clinic in Munich showing features of pneumonia. Neuropathological examination

of his brain revealed the wide-spread presence of amyloid plaques but not a

single neuron showing neurofibrillary change.

 

Alzheimer provides ample clinical, biographic and neuropathological

data of this patient which have allowed present scientists to identify

histological sections found among archival material at the Institute of

Neuropathology of the University of Munich. Using recently established methods for

the molecular genetic analysis of neuropathological tissue, it has been able to

perform mutational screening of exon 17 of the amyloid precursor protein (APP)

gene and genotyping for apolipoprotein E (APOE) alleles.

 

The history of this discovery in detail could be found at: M. B.

Graeber, S. Kosel, R. Egensperger, R. B. Banati, U. Muller, K. Bise, P. Hoff, H.

J. Moller, K. Fujisawa and P. Mehraein. Rediscovery of the case described by

Alois Alzheimer in 1911: historical, histological and molecular genetic analysis.

Neurogenetics 1997; 1 (1): 73–80.

On Mon, Sep 12, 2011 at 1:34 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

More clear version on historical aspect:

In 1907, Alzheimer published his now famous report on a 51- year-old

woman who had come under his care in 1901 while he worked as an attending

physician in the furt Asylum. The original case file of this patient,

Auguste D., was discovered recently, and it has been speculated that the

patient’s dementia was not caused by the typical neurodegeneration of Alzheimer

disease but by arteriosclerosis of the brain. Alzheimer’s report on Auguste D.

is not a full-size research paper but an abstract summarizing the presentation

he gave at the 37th Meeting of the Southwest German Psychiatrists in

Tubingen on November 3, 1906. Therefore, the first report by Alzheimer on the

morphology of the disease that was named after him by Emil Kraepelin in 1910 does

not contain any illustrations. Yet numerous figures, mainly drawings, which

include several examples of the histopathology of his first case were published

by Alzheimer in 1911 together with a second case report (Zbl. ges. Neurol.

Psych. 4: 356–385). In the report on his second published case, Alzheimer gives

a detailed description of the clinical history of a 56-year-old (Johann F.) who

suffered from presenile dementia and who was hospitalized in Kraepelin’s clinic

for more than 3 years. According to Alzheimer’s notes the patient was admitted

to the psychiatric clinic on November 12, 1907.

-------------------On Mon, Sep 12, 2011 at 1:13 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

Alois Alzheimer was born on 14th of June 1864

in Marktbreit am Main (Germany) and died in Breslau (now Wroclaw, Poland) on

December 19, 1915. Alzheimer’s most widely known contribution to the

Neurosciences is the histological description of the disease that was named latterly after

him by Emil Kraepelin. It was in Kraepelin’s clinic in Munich where Alzheimer’s life as a scientist came to full fruition. Following is the primary source reference:Kraepelin E (1910). Psychiatrie. Ein Lehrbuch für Studierende

und Ärzte. II. Band, Klinische Psychiatrie. Verlag Johann Ambrosius Barth, Leipzig.-----Syed Ziaur Rahman, MDSchool of MedicineUniversity of Western Sydney

AustraliaOn Mon, Sep 12, 2011 at 12:30 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

A very good morning to all NETRUMIANS. I am Mrinmoy Chakrabarty, from Dept. of Pharmacology, Veer Chandra Singh Garhwali Govt. Medical College and Research Institute, Srinagar, Pauri Garhwal, Uttarakhand. I am commencing a discussion on " RECENT ADVANCES IN ALZHEIMER'S RESEARCH " today and look forward to interacting with you on this theme. I expect to be able to cast light/ views on some of your queries or opinions and at the same time get stumped by the sheer insight of others. But then, that is the factor that spurs us to e- network for discussion on a topic. I felt a better discussion on the main theme would be facilitated with some information on few topics surrounding it and hence, am taking it up in a step wise manner with appropriate peripheral content.

1. Premise

Decades of research have proved futile to rein in the relentless progression of Alzheimer's disease (AD). With some of the most promising forerunner therapeutic molecules failing in late phase clinical trials lately and the existing modern therapies yielding only modest, short term benefits at the cost of different side effects, the scenario as of now is grim and looms large with the world burden of Alzheimer's slated to touch 65.7 million  mark by 2030 and 115.4 million by 2050.

The disease biology is still obscure with experts trying to have a better handle on the course of the disease progression. Every small detail is being re read, every single hypothesis scrutinized and every single notion re- considered to put together the pieces of the Alzheimer's puzzle.

 

2. A Brief History

AD was discovered in 1907 by Alois Alzheimer, but was not considered a major disease or disorder until the 1970s. Alzheimer documented a case of a woman in her fifties, August Deter who exhibited severe cognitive disorders pertaining to memory, language, and social interaction, according to Khachaturian and Radebaugh who have authored a book titled   " Alzheimer's disease: Cause(s), Diagnosis, Treatment, and Care. "

After the patient's death, Alzheimer performed an autopsy on her brain, using a silver staining technique that allowed him to visualize the neurons. In the process he found unusual formations, now known as amyloid plaques and neurofibrillary tangles. Alzheimer hypothesized that these lesions might be the cause or effect of the as yet to be named AD, or possibly a combination of the two. The disorder was later named after Alzheimer as more people were found to have the symptoms associated with his findings. 

In retrospect, before Alzheimer's 1907 discovery, scientists, clinicians and laymen took dementia as a " natural " progression of age, and " senility was accepted as a part of aging. "

Additionally, AD was not differentiated from other types of age-induced dementia or senility. AD did not suddenly " appear " in 1907, rather it was then that the disease was first recognized and named.

Even with Alzheimer's discovery, however, the disease was not one that was accepted as, well, a " disease. " Senility and dementia were still considered part of the aging process. Whaley states that AD did not become a common term, or even a large concern, until neurobiological research exploded in the late 1970s.

 

3. Dementia:

With a greater degree of prosperity setting in, we have a bigger ageing population to deal with and increasing age goes hand in hand with many of its attendant risks.

Dementia is one such prominent one for which we do not have a prevention, leave alone cure. It is defined as a generalized loss of cognitive abilities, including impairment of learning-memory with one or more of aphasia (defect or loss of power of expression by speech, writing, signs), apraxia (loss of ability to carry out familiar, purposeful movements, esp. inability to use objects correctly), agnosia (inability to recognize the import of sensory impressions e.g. auditory, gustatory, olfactory, tactile, visual), disturbed planning, organizing, abstract thinking abilities.

To simplify it is the loss of thinking, memory, and reasoning — that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that might accompany certain diseases or conditions. Symptoms also might include changes in personality, mood, and behaviour. Dementia is irreversible when caused by disease or injury, but might be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression.

Dementia develops when the parts of the brain that are involved with learning, memory, decision-making, and language are affected by any of various infections or diseases. The most common cause of dementia is AD, but there are as many as 50 other known causes.

Some of the disorders that cause dementia might be reversible, although unfortunately most types of dementia do not respond to treatment.

 

There are many causes of dementia but the most common causes include:

Degenerative neurological diseases, such as Alzheimer's, dementia with Lewy bodies, Parkinson's, and Huntington's

Vascular disorders, such as multiple-infarct dementia, which is causes by multiple strokes in the brain

Infections that affect the central nervous system, such as HIV dementia complex and Creutzfeldt-Jakob disease

Chronic drug use

Depression

Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from developmental abnormalities, infections, injury, or brain tumors

AD causes 50 percent to 70 percent of all dementia. However, researchers are finding that some of what was previously considered AD is really one of two other degenerative diseases: Lewy body disease and Pick's disease. There also are a number of other important disorders that can lead to dementia.

Dementia is considered a late-life disease because it tends to develop mostly in elderly people. About 5 percent to 8 percent of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. It is estimated that as many as half of people 85 or older suffer from dementia.

Dementia is not a disease; it is the clinical presentation or symptoms of a disease. In a nutshell, dementia is a symptom, and AD is the cause of the symptom.

4. Types of dementia

Although they are classified variedly based on different criteria, one of the broadest classifications based on the part of brain that is principally affected is

Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layers of the brain that play a critical role in cognitive processes such as learning,   memory and language. Alzheimer's and Creutzfeldt-Jakob disease are two forms of cortical dementia. Cortical dementia typically show severe memory impairment and aphasia.

 

Subcortical dementias result from dysfunction in the parts of the brain that are beneath the cortex. Usually, the memory loss and language difficulties that are characteristic of cortical dementias are not seen. Rather, people with subcortical dementias, such as Huntington's disease, Parkinson's Disease, and AIDS dementia complex, tend to show changes in their personality and attention span, stagnancy and slowing in thinking.

 

Treatable causes of dementia are reversible disorders that can be cured completely, or at least partially, by treating the underlying disorder. For example, dementia caused by any of the following are often at least partially treatable:

Chronic drug abuse

Tumours that can be removed

Subdural hematoma, an accumulation of blood beneath the outer covering of the brain that results from a broken blood vessel, usually as a result of a head injury (which can be minor and even unrecognized)

Normal pressure hydrocephalus

Metabolic disorders, such as a vitamin B12 deficiency

Hypothyroidism, a condition that results from low levels of thyroid secretion

Hypoglycemia, a condition that results from low blood sugar

Non-treatable causes of dementia include:

AD

Multi-infarct dementia

Dementias associated with Parkinson's disease and similar disorders

AIDS dementia complex

Creutzfeldt-Jakob disease (CJD), a quickly progressing and fatal disease that is characterized by dementia and myoclonus — muscle twitching and spasm

Since it is Day 1 of the discussion, we restrict ourselves to these generalized aspects and gradually move to the thick of Alzheimer's neurodegeneration in the days to come. Looking forward to your participation and Have A Great Day Ahead .

 

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

Dear Mrinmoy

The credit of all the information /

references that I shared goes to Professor B Graeber who is presently holding ‘Barnet-Cropper Chair

of Brain Tumor Research’ at Brain & Mind Research Institute (BMRI) of the Sydney Medical School, University of Sydney, and is also a good friend of me. He enlightened

me with all the good stories, anecdotes and history of Alois Alzheimer and his

lab. So, I can share more such historical aspects of Alois Alzheimer (at the

same time, I think past account of Alzheimer’s disease has already been enough in

the current discussion).

 

Professor Graeber earlier

worked at Max Planck Institute of Psychiatry, Department of Neuromorphology, Germany

and was close friend of Late Dr Parviz Mehraen (one of the student legacy of

Alois Alzheimer and himself a renowned neuroscientist from the Institute of

Neuropathology, Molecular Neuropathology Laboratory, Ludwig Maximilians

University, Munich, Germany. Parviz Mehraen originally from Iranian race of

Bahai faith (remember Lotus Temple at Delhi) actually published some of the original

works of Alois Alzheimer as he owned the lab of Alois Alzheimer latterly.

------------Syed Ziaur Rahman

On Mon, Sep 12, 2011 at 5:06 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

Good afternoon NETRUMIANS

Thank you so much Dr Rahman for filling us in on the background of AD. Surely, the discussion would be lacking without those comments of yours.

And yes, a special mention of Dr Biswas for pointing at inclusion of references. Actually, I was about to post the references at the end of the discussion and had compiled them in a separate file. But as pointed out by you, I will be including them at the end of each of my posts to the extent possible. It indeed undersores the veracity of the posts and also allows the readers to look up the particular sections of the theme in greater details as they wish. Looking forward to your further active cooperation in this discussion Dr Biswas.

TODAY'S REFERENCES

1) Berchtold NC, Cotman CW (1998). " Evolution in the conceptualization of dementia and Alzheimer's disease: Greco-Roman period to the 1960s " . Neurobiol. Aging 19 (3): 173–89.

2) Brookmeyer, R; , E; Ziegler-Graham, K; Arrighi, HM (2007). " Forecasting the global burden of Alzheimer's disease " . Alzheimer's and Dementia 3 (3): 186–91.

3) Holstein, M. " Alzheimer's Disease and Senile Dementia, 1885-1920: An Interpretive History of Disease Negot! iation. " Journal of Aging Studies. 1996, 11 (1): 1-13.

4) Whaley, S. " Senility, Confusion, Debate, Fear: Conceptualizing Alzheimer's Disease and the History of Senile Dementia. " Thesis. Drew University, Madison, NJ, 2002.

Good day !!!

Regards

Mrinmoy Chakrabarty

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

Thanks Dr Mrinmoy and Dr Rahman for such an interesting discussion. Yes if the references can be cited in short after each statement in the quoted text either with a number ( Vancouver Style ) or author name and year ( APA style) or even by a short url it would be very useful.

:-)On Mon, Sep 12, 2011 at 1:43 PM, Ibn Sina Academy <ibnsinaacademy@...> wrote:

 

Dear Mrinmoy

The credit of all the information /

references that I shared goes to Professor B Graeber who is presently holding ‘Barnet-Cropper Chair

of Brain Tumor Research’ at Brain & Mind Research Institute (BMRI) of the Sydney Medical School, University of Sydney, and is also a good friend of me. He enlightened

me with all the good stories, anecdotes and history of Alois Alzheimer and his

lab. So, I can share more such historical aspects of Alois Alzheimer (at the

same time, I think past account of Alzheimer’s disease has already been enough in

the current discussion).

 

Professor Graeber earlier

worked at Max Planck Institute of Psychiatry, Department of Neuromorphology, Germany

and was close friend of Late Dr Parviz Mehraen (one of the student legacy of

Alois Alzheimer and himself a renowned neuroscientist from the Institute of

Neuropathology, Molecular Neuropathology Laboratory, Ludwig Maximilians

University, Munich, Germany. Parviz Mehraen originally from Iranian race of

Bahai faith (remember Lotus Temple at Delhi) actually published some of the original

works of Alois Alzheimer as he owned the lab of Alois Alzheimer latterly.

------------Syed Ziaur Rahman

On Mon, Sep 12, 2011 at 5:06 PM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

Good afternoon NETRUMIANS

Thank you so much Dr Rahman for filling us in on the background of AD. Surely, the discussion would be lacking without those comments of yours.

And yes, a special mention of Dr Biswas for pointing at inclusion of references. Actually, I was about to post the references at the end of the discussion and had compiled them in a separate file. But as pointed out by you, I will be including them at the end of each of my posts to the extent possible. It indeed undersores the veracity of the posts and also allows the readers to look up the particular sections of the theme in greater details as they wish. Looking forward to your further active cooperation in this discussion Dr Biswas.

TODAY'S REFERENCES

1) Berchtold NC, Cotman CW (1998). " Evolution in the conceptualization of dementia and Alzheimer's disease: Greco-Roman period to the 1960s " . Neurobiol. Aging 19 (3): 173–89.

2) Brookmeyer, R; , E; Ziegler-Graham, K; Arrighi, HM (2007). " Forecasting the global burden of Alzheimer's disease " . Alzheimer's and Dementia 3 (3): 186–91.

3) Holstein, M. " Alzheimer's Disease and Senile Dementia, 1885-1920: An Interpretive History of Disease Negot! iation. " Journal of Aging Studies. 1996, 11 (1): 1-13.

4) Whaley, S. " Senility, Confusion, Debate, Fear: Conceptualizing Alzheimer's Disease and the History of Senile Dementia. " Thesis. Drew University, Madison, NJ, 2002.

Good day !!!

Regards

Mrinmoy Chakrabarty

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

The 2011 World Alzheimer Report has been produced by

Alzheimer's Disease International and was put together by a team of researchers

from King's College London Institute of Psychiatry. It found that at least half

of dementia sufferers in richer countries aren't being diagnosed, and in poorer

countries that figure is far worse. Overall, the report says 28 million of the

world's 36 million dementia sufferers haven't been diagnosed. The chairperson

of Alzheimer's Disease International, Dr Daisy Acosta says the figures are sad

because treatments and interventions work better in the earlier stages of

dementia.Source: http://www.alz.co.uk/research/world-report

------------------Syed Ziaur RahmanOn Wed, Sep 14, 2011 at 12:21 AM, mrinmoychakrabarty <mrinmoychakrabarty@...> wrote:

 

12th INTERNATIONAL CONFERENCE ON ALZHEIMER'S DRUG DISCOVERY

September 26-27, 2011  •  Jersey City, NJ, USA (across from NYC on the Hudson)

http://www.worldeventsforum.com/addf/addrugdiscovery/

-- Ibn Sina Academy of Medieval Medicine & SciencesTijara House, Dodhpur, Aligarh 202002, Indiaweb link: www.ibnsinaacademy.org

Join us on Facebook: http://www.facebook.com/IAMMS.AligarhFollow us on Twitter: http://twitter.com/Ibnsinaacademy

 

[Guest guest]

Are we following this discussion?

Hi my young NetRUMians.

By the time we grow old, some of us may have to read about recent advances in

Alzheimer therapy for our self use. Our young moderator Mrinmoy is indeed

handling the topic with great stealth and determination. But unfortunately very

few are interacting. May we see greater participation from the members please?

Earnestly,

Vijay

>

> Dear Memebers

>

> In today's post, amyloid beta appears as amyloid I raised to power 2. It is an

inadvertent error that crept in while formatting and typesetting the text with

rich text editor after it was pasted from the original source document I had

prepared for moderation on the aforesaid theme.

>

> I apologise the same and would be careful about proof reading future posts

>

> Regards

>

> Mrinmoy Chakrabarty

>

[Guest guest]

I do follow the discussion.Non-participation - may be many us are old enough and in the threshold of Alzheimer's.we rather remember to forget (and forget to remember too)Nice presentation. congrats to the author & moderator.G SivagnanamFrom: Vijay <drvijaythawani@...>netrum Sent: Thursday, September 15, 2011 5:13

AMSubject: Re: RECENT ADVANCES IN ALZHEIMER'S RESEARCH

Are we following this discussion?

Hi my young NetRUMians.

By the time we grow old, some of us may have to read about recent advances in Alzheimer therapy for our self use. Our young moderator Mrinmoy is indeed handling the topic with great stealth and determination. But unfortunately very few are interacting. May we see greater participation from the members please?

Earnestly,

Vijay

>

> Dear Memebers

>

> In today's post, amyloid beta appears as amyloid I raised to power 2. It is an inadvertent error that crept in while formatting and typesetting the text with rich text editor after it was pasted from the original source document I had prepared for moderation on the aforesaid theme.

>

> I apologise the same and would be careful about proof reading future posts

>

> Regards

>

> Mrinmoy Chakrabarty

>

[Guest guest]

World Federation For Neuro Rehabilitation, Melbourne, Australia

16-19 May. 2012.

https://www.dcconferences.com.au/wcnr2012/