wow!!!...check this out...Reversal Of Alzheimer's Symptoms Within Minutes In Human Study...(so is this applicable to Ds, too?? read both articles.)...

[Guest guest]

http://www.sciencedaily.com/releases/2008/01/080109091102.htm

Reversal Of Alzheimer's Symptoms Within

Minutes In Human Study

ScienceDaily (Jan. 9, 2008) — An

extraordinary new scientific study, which for the first time documents marked

improvement in Alzheimer’s disease within minutes of administration of a

therapeutic molecule, has just been published in the Journal of

Neuroinflammation.

This new study highlights the importance of certain soluble proteins, called

cytokines, in Alzheimer’s disease. The study focuses on one of these

cytokines, tumor necrosis factor-alpha(TNF), a critical component of the

brain’s immune system. Normally, TNF finely regulates the transmission of

neural impulses in the brain. The authors hypothesized that elevated levels of

TNF in Alzheimer’s disease interfere with this regulation. To reduce

elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic

called etanercept. Excess TNF-alpha has been documented in the cerebrospinal

fluid of patients with Alzheimer’s.

The new study documents a dramatic and unprecedented therapeutic effect in

an Alzheimer’s patient: improvement within minutes following delivery of

perispinal etanercept, which is etanercept given by injection in the spine.

Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is

FDA approved to treat a number of immune-mediated disorders and is used off

label in the study.

The use of anti-TNF therapeutics as a new treatment choice for many

diseases, such as rheumatoid arthritis and potentially even Alzheimer’s,

was recently chosen as one of the top 10 health stories of 2007 by the Harvard

Health Letter.

Similarly, the Neurotechnology Industry Organization has recently selected

new treatment targets revealed by neuroimmunology (such as excess TNF) as one

of the top 10 Neuroscience Trends of 2007. And the Dana Alliance for Brain

Initiatives has chosen the pilot study using perispinal etanercept for

Alzheimer’s for inclusion and discussion in their 2007 Progress Report on

Brain Research.

The lead author of the study, Tobinick M.D., is an assistant clinical

professor of medicine at the University of California, Los Angeles and director

of the Institute for Neurological Research, a private medical group in Los

Angeles. Hyman Gross, M.D., clinical professor of neurology at the University

of Southern California, was co-author.

The study is accompanied by an extensive commentary by Sue , Ph.D.,

director of research at the W. Reynolds Institute on Aging at the

University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the

Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who

along with Mrak, M.D., chairman of pathology at University of Toledo

Medical School, are editors-in-chief of the Journal of Neuroinflammation.

and Mrak are pioneers in the field of neuroinflammation.

published a landmark study in 1989 describing the association of cytokine

overexpression in the brain and Alzheimer’s disease. Her research helped

pave the way for the findings of the present study. has recently been

selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit

organization of more than 200 leading neuroscientists, including ten Nobel

laureates.

“It is unprecedented that we can see cognitive and behavioral

improvement in a patient with established dementia within minutes of

therapeutic intervention,” said . “It is imperative that the

medical and scientific communities immediately undertake to further investigate

and characterize the physiologic mechanisms involved. This gives all of us in

Alzheimer’s research a tremendous new clue about new avenues of research,

which is so exciting and so needed in the field of Alzheimer’s. Even

though this report predominantly discusses a single patient, it is of

significant scientific interest because of the potential insight it may give

into the processes involved in the brain dysfunction of Alzheimer’s.”

While the article discusses one patient, many other patients with mild to

severe Alzheimer’s received the treatment and all have shown sustained

and marked improvement.

The new study, entitled “Rapid cognitive improvement in

Alzheimer’s disease following perispinal etanercept

administration,” and the accompanying commentary, entitled

“Perispinal etanercept: Potential as an Alzheimer’s

therapeutic,” are available on the Web site of the Journal of

Neuroinflammation (http://www.jneuroinflammation.com/content/5/1/2/abstract).

Author Hyman Gross, M.D., has no competing interests. Author

Tobinick, M.D. owns stock in Amgen, the manufacturer of etanercept, and has

multiple issued and pending patents assigned to TACT IP LLC that describe the

parenteral and perispinal use of etanercept for the treatment of

Alzheimer’s disease and other neurological disorders, including, but not

limited to, U.S. patents 6015557, 6177077, 6419934, 6419944, 6537549, 6982089,

7214658 and Australian patent 758523.

Adapted from materials provided by University of Arkansas for Medical Sciences.

Now check this out:

http://tinyurl.com/2r7xyu

Neurobiology of Aging

Volume 26, Issue 3,

March 2005, Pages 349-354

Developmental Origins of Aging in the Brain and Blood Vessels

Abstract

Full Text + Links

PDF (121 K)

Cited

By in Scopus (71)

Copyright © 2004 Elsevier Inc. All

rights reserved.

Glia and their cytokines in progression of neurodegeneration

E. Mraka, d and W. Sue T.

b, c, d, e, ,

aDepartment of Pathology, University of Arkansas

for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205,

USA

b W. Reynolds Department of Geriatrics,

University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103,

Little Rock, AR 72205, USA

cDepartment of Physiology, University of Arkansas

for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205,

USA

dDepartment of Neurobiology and Developmental

Sciences, University of Arkansas for Medical Sciences, 629 South Elm Street,

Room 3103, Little Rock, AR 72205, USA

eGeriatric Research Education Clinical Center, Central

Arkansas Veterans HealthCare System, Little Rock, AR 72205, USA

Received 19 December 2003; revised 3 May 2004; accepted 4 May

2004. Available online 10 December 2004.

Abstract

A glia-mediated, inflammatory immune response is an important component of

the neuropathophysiology of Alzheimer's disease, of the midlife

neurodegeneration of Down's syndrome, and of other age-related

neurodegenerative conditions. All of these conditions are associated with early

and often dramatic activation of, and cytokine overexpression in, microglia and

astrocytes, sometimes decades before pathological changes consistent with a

diagnosis of Alzheimer's disease are apparent, as in patients with Down's

syndrome or head injury. Brains of normal elderly individuals also often show

Alzheimer-type neuropathological changes, although to a lesser degree than

those seen in Alzheimer's disease itself. These normal age-related glial

changes, likely a response to the normal wear and tear of the aging process,

raise the threshold of glial activation and thus may explain the fact that even

genetically determined Alzheimer's disease, resulting from genetic mutations

such as those in â-amyloid precursor protein and presenilins or from genetic

duplication such as of chromosome 21, only shows the full manifestation of the

disease decades after birth. In the more common sporadic form of Alzheimer's

disease, age-related increases in glial activation and expression of cytokines

may act in synergy with other genetic and acquired environmental risks to

culminate in the development of disease.

Keywords: Glia; Cytokines; Neurodegeneration

Corresponding

author. Tel.: +1 501 526 5800; fax: +1 501 526 5830.

 search & _sort=d & view=c & _acct=C000050221 & _version=1 & _urlVersion=0 & _userid=10 & md5=9eb5e6264bd2ea97692c26f66f1b6650

[Guest guest]

Wow...this stuff is used as a treatment for Inflammatory Bowel Disease like has. Hmmmm...maybe I'd better look into it further. Thanks for posting kathy.

Sherry

[Guest guest]

Thank you so much for posting this. One of the scientist at Stanford on the DS team is studying TNF. This may be a fantastic break through. Kathy Ratkiewicz <Kathy_R@...> wrote: http://www.sciencedaily.com/releases/2008/01/080109091102.htm Reversal Of

Alzheimer's Symptoms Within Minutes In Human Study ScienceDaily (Jan. 9, 2008) — An extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer’s disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation. This new study highlights the importance of certain soluble proteins, called cytokines, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a critical component of the brain’s immune system. Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimer’s disease interfere with this regulation. To reduce elevated TNF, the authors gave

patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer’s. The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used off label in the study. The use of anti-TNF therapeutics as a new treatment choice for many diseases, such as rheumatoid arthritis and potentially even Alzheimer’s, was recently chosen as one of the top 10 health stories of 2007 by the Harvard Health Letter. Similarly, the Neurotechnology Industry Organization has recently selected new treatment targets revealed by neuroimmunology (such as

excess TNF) as one of the top 10 Neuroscience Trends of 2007. And the Dana Alliance for Brain Initiatives has chosen the pilot study using perispinal etanercept for Alzheimer’s for inclusion and discussion in their 2007 Progress Report on Brain Research. The lead author of the study, Tobinick M.D., is an assistant clinical professor of medicine at the University of California, Los Angeles and director of the Institute for Neurological Research, a private medical group in Los Angeles. Hyman Gross, M.D., clinical professor of neurology at the University of Southern California, was co-author. The study is accompanied by an extensive commentary by Sue , Ph.D., director of research at the W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who along with Mrak, M.D., chairman of

pathology at University of Toledo Medical School, are editors-in-chief of the Journal of Neuroinflammation. and Mrak are pioneers in the field of neuroinflammation. published a landmark study in 1989 describing the association of cytokine overexpression in the brain and Alzheimer’s disease. Her research helped pave the way for the findings of the present study. has recently been selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit organization of more than 200 leading neuroscientists, including ten Nobel laureates. “It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention,” said . “It is imperative that the medical and scientific communities immediately undertake to further investigate and characterize the physiologic mechanisms involved. This gives all of us in Alzheimer’s research

a tremendous new clue about new avenues of research, which is so exciting and so needed in the field of Alzheimer’s. Even though this report predominantly discusses a single patient, it is of significant scientific interest because of the potential insight it may give into the processes involved in the brain dysfunction of Alzheimer’s.” While the article discusses one patient, many other patients with mild to severe Alzheimer’s received the treatment and all have shown sustained and marked improvement. The new study, entitled “Rapid cognitive improvement in Alzheimer’s disease following perispinal etanercept administration,” and the accompanying commentary, entitled “Perispinal etanercept: Potential as an Alzheimer’s therapeutic,” are available on the Web site of the Journal of Neuroinflammation (http://www.jneuroinflammation.com/content/5/1/2/abstract). Author Hyman Gross, M.D., has no competing interests. Author Tobinick, M.D. owns stock in Amgen, the manufacturer of etanercept, and has multiple issued and pending patents assigned to TACT IP LLC that describe the parenteral and perispinal use of etanercept for the treatment of Alzheimer’s disease and other neurological disorders, including, but not limited to, U.S. patents 6015557, 6177077, 6419934, 6419944, 6537549, 6982089, 7214658 and Australian patent 758523. Adapted from materials provided by University of Arkansas for Medical Sciences. Now check this out: http://tinyurl.com/2r7xyu Neurobiology of Aging Volume 26, Issue 3, March 2005, Pages 349-354 Developmental Origins of Aging in the Brain and Blood Vessels Abstract Full Text + Links PDF (121 K) Cited By in Scopus (71) Copyright © 2004 Elsevier Inc. All rights reserved. Glia and their cytokines in progression of neurodegeneration E. Mraka, d and W. Sue T. b, c, d, e, , aDepartment of Pathology, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USAb W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USAcDepartment of Physiology, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USAdDepartment of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USAeGeriatric Research Education Clinical Center, Central Arkansas Veterans HealthCare System, Little Rock, AR 72205, USA Received 19 December 2003; revised 3 May 2004; accepted 4 May 2004. Available online 10 December 2004. Abstract A glia-mediated, inflammatory immune response is an important component of the neuropathophysiology of Alzheimer's disease, of the

midlife neurodegeneration of Down's syndrome, and of other age-related neurodegenerative conditions. All of these conditions are associated with early and often dramatic activation of, and cytokine overexpression in, microglia and astrocytes, sometimes decades before pathological changes consistent with a diagnosis of Alzheimer's disease are apparent, as in patients with Down's syndrome or head injury. Brains of normal elderly individuals also often show Alzheimer-type neuropathological changes, although to a lesser degree than those seen in Alzheimer's disease itself. These normal age-related glial changes, likely a response to the normal wear and tear of the aging process, raise the threshold of glial activation and thus may explain the fact that even genetically determined Alzheimer's disease, resulting from genetic mutations such as those in â-amyloid precursor protein and presenilins or from genetic duplication such as of chromosome 21, only shows the full

manifestation of the disease decades after birth. In the more common sporadic form of Alzheimer's disease, age-related increases in glial activation and expression of cytokines may act in synergy with other genetic and acquired environmental risks to culminate in the development of disease. Keywords: Glia; Cytokines; Neurodegeneration Corresponding author. Tel.: +1 501 526 5800; fax: +1 501 526 5830. search & _sort=d & view=c & _acct=C000050221 & _version=1 & _urlVersion=0 & _userid=10 & md5=9eb5e6264bd2ea97692c26f66f1b6650

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