Liver, Not Brain, May Be Origin of Alzheimer’s Plaques

[n2doc]

ScienceDaily (Mar. 3, 2011) — Unexpected results from a Scripps Research Institute and ModGene, LLC study could completely alter scientists' ideas about Alzheimer's disease -- pointing to the liver instead of the brain as the source of the "amyloid" that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment.

The study was published online March 3 in The Journal of Neuroscience Research.

In the study, the scientists used a mouse model for Alzheimer's disease to identify genes that influence the amount of amyloid that accumulates in the brain. They found three genes that protected mice from brain amyloid accumulation and deposition. For each gene, lower expression in the liver protected the mouse brain. One of the genes encodes presenilin -- a cell membrane protein believed to contribute to the development of human Alzheimer's.

"This unexpected finding holds promise for the development of new therapies to fight Alzheimer's," said Scripps Research Professor Greg Sutcliffe, who led the study. "This could greatly simplify the challenge of developing therapies and prevention."

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http://www.sciencedaily.com/releases/2011/03/110303134435.htm

[no_hypocrisy]

1. The article doesn't address whether the liver manifestation is due to

particular foods and drinks ingested or whether it's an independent phenomenon, i.e., genetics.

[n2doc]

2. Since it is in a mouse model it is genetic

And other causes in humans would still need to be investigated. This is but one pathway.

[Name removed]

3. Deleted message

Message removed by moderator. Click here to review the message board rules.

[HysteryDiagnosis]

4. In some way or another this should relate, mebbe not. DHA does affect where

proteins are cleaved in the brain and I believe this fact was posted before.

Deficient liver biosynthesis of docosahexaenoic acid correlates with cognitive impairment in Alzheimer's disease.

Astarita G, Jung KM, Berchtold NC, Nguyen VQ, Gillen DL, Head E, Cotman CW, Piomelli D.

Department of Pharmacology, University of California Irvine, Irvine, California, United States of America.
Abstract

Reduced brain levels of docosahexaenoic acid (C22:6n-3), a neurotrophic and neuroprotective fatty acid, may contribute to cognitive decline in Alzheimer's disease. Here, we investigated whether the liver enzyme system that provides docosahexaenoic acid to the brain is dysfunctional in this disease. Docosahexaenoic acid levels were reduced in temporal cortex, mid-frontal cortex and cerebellum of subjects with Alzheimer's disease, compared to control subjects (P  =  0.007). Mini Mental State Examination (MMSE) scores positively correlated with docosahexaenoic/α-linolenic ratios in temporal cortex (P =  0.005) and mid-frontal cortex (P  =  0.018), but not cerebellum. Similarly, liver docosahexaenoic acid content was lower in Alzheimer's disease patients than control subjects (P  =  0.011).

Liver docosahexaenoic/α-linolenic ratios correlated positively with MMSE scores (r  =  0.78; P<0.0001), and negatively with global deterioration scale grades (P  =  0.013). Docosahexaenoic acid precursors, including tetracosahexaenoic acid (C24:6n-3), were elevated in liver of Alzheimer's disease patients (P  =  0.041), whereas expression of peroxisomal d-bifunctional protein, which catalyzes the conversion of tetracosahexaenoic acid into docosahexaenoic acid, was reduced (P  = 0.048). Other genes involved in docosahexaenoic acid metabolism were not affected.

The results indicate that a deficit in d-bifunctional protein activity impairs docosahexaenoic acid biosynthesis in liver of Alzheimer's disease patients, lessening the flux of this neuroprotective fatty acid to the brain.