Alzheimer's-like brain changes seen in young who breathed polluted air

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ehn synopsis:

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Alzheimer's-like brain changes seen in young who breathed polluted

air.

<http://www.environmentalhealthnews.org/ehs/newscience/2011/12/2011-1227-air-pol\

lution-alzheimers-young-adults/>

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* 30 January 2012

Children and young adults from areas with highly polluted air in

Mexico had physical and genetic changes in their brains akin to

those found in adults with Alzheimer's disease. The changes seen are

surprising because they are not supposed to occur in younger brains.

Over half of the brains from the urban areas showed signs of

amyloid-B plaques and 40 percent had pretangle material. In

contrast, none of the brains from the rural areas had either condition.

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more...

<http://www.environmentalhealthnews.org/ehs/newscience/2011/12/2011-1227-air-pol\

lution-alzheimers-young-adults/>

eg Residential proximity to freeways and autism in the CHARGE study.

<http://www.ncbi.nlm.nih.gov/pubmed/21156395>

Volk HE, Hertz-Picciotto I, Delwiche L, Lurmann F, McConnell R.

Environ Health Perspect. 2011 Jun;119(6):873-7.

Increased secreted amyloid precursor protein-? (sAPP?) in severe autism:

proposal of a specific, anabolic pathway and putative biomarker.

<http://www.ncbi.nlm.nih.gov/pubmed/21731612>

Ray B, Long JM, Sokol DK, Lahiri DK.

PLoS One. 2011;6(6):e20405.

Peripheral biomarkers in Autism: secreted amyloid precursor

protein-alpha as a probable key player in early diagnosis.

<http://www.ncbi.nlm.nih.gov/pubmed/19079679>

AR, Giunta BN, Obregon D, Nikolic WV, Tian J, Sanberg CD, Sutton

DT, Tan J.

Int J Clin Exp Med. 2008;1(4):338-44.

High levels of Alzheimer beta-amyloid precursor protein (APP) in

children with severely autistic behavior and aggression.

<http://www.ncbi.nlm.nih.gov/pubmed/16948926>

Sokol DK, Chen D, Farlow MR, Dunn DW, Maloney B, Zimmer JA, Lahiri DK.

J Child Neurol. 2006 Jun;21(6):444-9.

Neuropathological observations in a case of autism presenting with

self-injury behavior. <http://www.ncbi.nlm.nih.gov/pubmed/1759563>

Hof PR, Knabe R, Bovier P, Bouras C.

Acta Neuropathol. 1991;82(4):321-6.

We report the neuropathological evaluation of a 24-year-old autistic

woman suffering from a residual state of infantile autism and presenting

with self-injury behavior since childhood. Her behavior included

head-banging, eye-gouging and self-biting. All intended therapeutic

measures remained without effect, including high doses of psychotropic

drugs. At autopsy, numerous /neurofibrillary tangles/ were found in the

perirhinal and entorhinal cortex where they were frequently grouped in

nests or clusters. A few neurofibrillary tangles were also observed in

the amygdala and in the prepiriform and orbito-frontal cortex. In the

cortex, tangles were located in both layers II and III. There were no

neuritic plaques or amyloid deposits. Interestingly, neurofibrillary

tangles have been described in brains of individuals who had experienced

repeated head injuries such as boxers (dementia pugilistica) and soccer

players, suggesting that in our case a similar mechanism induced tangle

formation and resulted in the loss of selective neuronal populations.

The molecular biology of senile plaques and neurofibrillary tangles in

Alzheimer's disease. <http://www.ncbi.nlm.nih.gov/pubmed/20054780>

Armstrong RA.

Folia Neuropathol. 2009;47(4):289-99.

Since the earliest descriptions of the disease, senile plaques (SP) and

neurofibrillary tangles (NFT) have been regarded as the pathological

'hallmarks' of Alzheimer's disease (AD). Whether or not SP and NFT are

sufficient cause to explain the neurodegeneration of AD is

controversial. The major molecular constituents of these lesions, viz.,

beta-amyloid (Ass) and tau, have played a defining role both in the

diagnosis of the disease and in studies of pathogenesis. The molecular

biology of SP and NFT, however, is complex with many chemical

constituents. An individual constituent could be the residue of a

pathogenic gene mutation, result from cellular degeneration, or reflect

the acquisition of new proteins by diffusion and molecular binding. This

review proposes that the molecular composition of SP and NFT is largely

a consequence of cell degeneration and the later acquisition of

proteins. Such a conclusion has implications both for the diagnosis of

AD and in studies of disease pathogenesis.