Alzheimer's a form of diabetes?

[Guest guest]

An item from Dr. Mirkin follows,along with the abstract of the

article he cited.

Mike

Mirkin:

A study from Brown University Medical School shows

that Alzheimers disease may be another form of diabetes, and

all the recommendations for avoiding diabetes may also protect

your memory (Journal of Alzheimer's Disease, November 2005.)

Like the pancreas, the brain produces insulin. Professor Suzanne

M. de la Monte showed that brain levels of insulin and insulin

receptors fall during the early stages of Alzheimer's and continue

to drop progressively as the disease progresses. Other features

of Alzheimer's, such as cell death and tangles in the brain, could

be caused by abnormalities in insulin functions.

Furthermore, lack of insulin lowers brain levels of the

neurotransmitter acetylcholine, which is seen regularly in

Alzheimer's disease. This would explain why every factor known

to increase risk for heart attacks also increases risk for

Alzheimers disease. Even though these studies are preliminary,

it is a good idea to reduce susceptibility to developing diabetes

by markedly reducing your intake of sugar and flour; increasing

your intake of fruits, vegetable, whole grains, beans, and nuts;

avoiding weight gain and exercising regularly. See

http://www.drmirkin.com/diabetes/1555.html

Abstract and Tiny URL:

Insulin and insulin-like growth factor expression and function

deteriorate with progression of Alzheimer's disease: Link to brain

reductions in acetylcholine

Enrique J. A1, Alison Goldin A1, Noah Fulmer A1, Rose Tavares

A1, Jack R. Wands A1, Suzanne M. de la Monte A1

A1 Departments of Pathology and Medicine, Rhode Island Hospital and

Brown Medical School, Providence, RI, USA

Reduced glucose utilization and energy metabolism occur early in the

course of Alzheimer's disease (AD) and correlate with impaired

cognition. Glucose utilization and energy metabolism are regulated

by insulin and insulin-like growth factor I (IGF-I), and

correspondingly, studies have shown that cognitive impairment may be

improved by glucose or insulin administration. Recently, we

demonstrated significantly reduced levels of insulin and IGF-I

polypeptide genes and their corresponding receptors in advanced AD

relative to aged control brains. The abnormalities in gene

expression were accompanied by impaired survival signaling

downstream through PI3 kinase-Akt. The present work characterizes

the abnormalities in insulin and IGF gene expression and receptor

binding in brains with different Braak stage severities of AD.

Realtime quantitative RT-PCR analysis of frontal lobe tissue

demonstrated that increasing AD Braak Stage was associated with

progressively reduced levels of mRNA corresponding to insulin, IGF-

I, and IGF-II polypeptides and their receptors, tau, which is

regulated by insulin and IGF-I, and the Hu D neuronal RNA binding

protein. In contrast, progressively increased levels of amyloid â

protein precursor (AâPP), glial fibrillary acidic protein, and the

IBA1/AIF1 microglial mRNA transcripts were detected with increasing

AD Braak Stage. Impairments in growth factor and growth factor

receptor expression and function were associated with increasing AD

Braak stage dependent reductions in insulin, IGF-I, and IGF-II

receptor binding, ATP levels, and choline acetyltransferase (ChAT)

expression. Further studies demonstrated that: 1) ChAT expression

increases with insulin or IGF-I stimulation; 2) ChAT is expressed in

insulin and IGF-I receptor-positive cortical neurons; and 3) ChAT co-

localization in insulin or IGF-I receptor-positive neurons is

reduced in AD. Together, these data provide further evidence that AD

represents a neuro-endocrine disorder that resembles a unique form

of diabetes mellitus (? Type 3) and progresses with severity of

neurodegeneration.

http://tinyurl.com/dnfxx