EVIDENCE SUGGESTS ALZHEIMER'S MAY BE A TYPE OF DIABETES

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EVIDENCE SUGGESTS ALZHEIMER'S MAY BE A TYPE OF DIABETES

Science Blog

November 30, 2005

http://www.scienceblog.com/cms/evidence_suggests_alzheimers_may_be_a_type_of

_diabetes_9394

Researchers at Rhode Island Hospital and Brown Medical School have

discovered that insulin and its receptors drop significantly in the brain

during the early stages of Alzheimer's disease, and that levels decline

progressively as the disease becomes more severe, leading to further

evidence that Alzheimer's is a new type of diabetes. They also found that

acetylcholine deficiency, a hallmark of the disease, is linked directly to

the loss of insulin and insulin-like growth factor function in the brain.

The study, published in the November issue of the Journal of Alzheimer's

Disease (http://www.j-alz.com), is the first to look at insulin levels early

in the course of the disease. The authors' previous work published earlier

this year primarily focused on the late stages of Alzheimer's.

" Insulin disappears early and dramatically in Alzheimer's disease. And many

of the unexplained features of Alzheimer's, such as cell death and tangles

in the brain, appear to be linked to abnormalities in insulin signaling.

This demonstrates that the disease is most likely a neuroendocrine disorder,

or another type of diabetes, " says senior author Suzanne M. de la Monte, a

neuropathologist at Rhode Island Hospital and a professor of pathology at

Brown Medical School in Providence, RI.

The study analyzed postmortem brain tissue of 45 patients with a diagnosis

of either normal aging or different degrees of Alzheimer's

neurodegeneration, termed " Braak Stages. " Researchers analyzed insulin and

insulin receptor function in the frontal cortex, a major area affected by

Alzheimer's. They found that with increasing severity of the disease, levels

of insulin receptors and the brain's ability to respond to insulin decreased

markedly.

" In the most advanced stage of Alzheimer's, insulin receptors were nearly 80

percent lower than in a normal brain, " de la Monte says.

Researchers found two parallel abnormalities related to insulin in

Alzheimer's. First, insulin levels decline as the disease progresses.

Second, insulin and its related protein IGF-I lose their ability to bind to

corresponding cell receptors, creating a resistance to the growth factors

and thus causing cells to malfunction and eventually die.

" This has important implications for treatment, " de la Monte says. " If you

could target the disease early, you could prevent the further loss of

neurons. But you would have to target not just the loss of insulin but the

resistance of its receptors in the brain. "

Researchers also offer an explanation for the acetylcholine deficiency that

is linked to dementia and has long been recognized as an early abnormality

in Alzheimer's. They found that insulin and IGF-I stimulate the expression

of choline acetyltransferase (ChAT), the enzyme responsible for making

acetylcholine. This discovery shows a direct link between insulin and IGF-I

deficiency and dementia.

" We're able to show that insulin impairment happens early in the disease.

We're able to show it's linked to major neurotransmitters responsible for

cognition. We're able to show it's linked to poor energy metabolism, and

it's linked to abnormalities that contribute to the tangles characteristic

of advanced Alzheimer's disease. This work ties several concepts together,

and demonstrates that Alzheimer's disease is quite possibly a Type 3

diabetes, " de la Monte says.

Earlier this year, de la Monte and co-authors provided the first evidence

that insulin and its related proteins are produced in the brain and that

reduced levels of both are linked to the late stages of Alzheimer's. They

surmised that Alzheimer's is a complex neuroendocrine disease that

originates in the central nervous system, raising the possibility of a new

type of diabetes.

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