Re: Alzheimer's a form of diabetes?

[Guest guest]

Hi folks:

This is good stuff. And, if correct, excellent news because it

suggests we are much less likely than average ever to suffer

alzheimer's.

However, if it is true then why is it that I have never heard anyone

claim, nor ever seen data that show, that alzheimer's is incredibly

common among diabetics? Is it? And if it isn't, why not?

Rodney.

--- In , " mikesheldrick " <mike@s...>

wrote:

>

> 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

>

[Guest guest]

Hi folks:

This is good stuff. And, if correct, excellent news because it

suggests we are much less likely than average ever to suffer

alzheimer's.

However, if it is true then why is it that I have never heard anyone

claim, nor ever seen data that show, that alzheimer's is incredibly

common among diabetics? Is it? And if it isn't, why not?

Rodney.

--- In , " mikesheldrick " <mike@s...>

wrote:

>

> 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

>