Re: Re: Alzheimer's a form of diabetes?

[Guest guest]

I would guess it does:

The Lancet NeurologyVolume 5 • Number 1 • January 2006Copyright © 2006

ReviewRisk of dementia in diabetes mellitus: a systematic review

Although the association between diabetes and these modest changes in cognition is now well established, the relation between diabetes and dementia is an area of controversy. Early studies that reported a low rate of diabetes in patients with Alzheimer's disease,8, 9, 10 suggested that diabetes and Alzheimer's disease might not coexist.9 However, a more recent study suggested that type 2 diabetes or impaired fasting glucose might be present in up to 80% of patients with Alzheimer's disease.11

11 Janson J, Laedtke T, Parisi JE, O'Brien P, sen RC, PC, Increased risk of type 2 diabetes in Alzheimer disease . Diabetes (2004) 53 : pp 474-481 .

Increased risk of type 2 diabetes in Alzheimer disease.Janson J - Diabetes - 01-FEB-2004; 53(2): 474-81From NIH/NLM MEDLINE

NLM Citation ID:14747300 (PubMed)

Full Source Title:Diabetes

Author Affiliation:Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota, USA.

Authors:Janson J; Laedtke T; Parisi JE; O'Brien P; sen RC; PC

Abstract:Alzheimer disease and type 2 diabetes are characterized by increased prevalence with aging, a genetic predisposition, and comparable pathological features in the islet and brain (amyloid derived from amyloid beta protein in the brain in Alzheimer disease and islet amyloid derived from islet amyloid polypeptide in the pancreas in type 2 diabetes). Evidence is growing to link precursors of amyloid deposition in the brain and pancreas with the pathogenesis of Alzheimer disease and type 2 diabetes, respectively. Given these similarities, we questioned whether there may be a common underlying mechanism predisposing to islet and cerebral amyloid. To address this, we first examined the prevalence of type 2 diabetes in a community-based controlled study, the Mayo Clinic Alzheimer Disease Patient Registry (ADPR), which follows patients with Alzheimer disease versus control subjects without Alzheimer disease. In addition to this clinical study, we performed a pathological study of autopsy cases from this same community to determine whether there is an increased prevalence of islet amyloid in patients with Alzheimer disease and increased prevalence of cerebral amyloid in patients with type 2 diabetes. Patients who were enrolled in the ADPR (Alzheimer disease n = 100, non-Alzheimer disease control subjects n = 138) were classified according to fasting glucose concentration (FPG) as nondiabetic (FPG <110 mg/dl), impaired fasting glucose (IFG, FPG 110-125 mg/dl), and type 2 diabetes (FPG >126 mg/dl). The mean slope of FPG over 10 years in each case was also compared between Alzheimer disease and non-Alzheimer disease control subjects. Pancreas and brain were examined from autopsy specimens obtained from 105 humans (first, 28 cases of Alzheimer disease disease vs. 21 non-Alzheimer disease control subjects and, second, 35 subjects with type 2 diabetes vs. 21 non-type 2 diabetes control subjects) for the presence of islet and brain amyloid. Both type 2 diabetes (35% vs. 18%; P < 0.05) and IFG (46% vs. 24%; P < 0.01) were more prevalent in Alzheimer disease versus non-Alzheimer disease control subjects, so 81% of cases of Alzheimer disease had either type 2 diabetes or IFG. The slope of increase of FPG with age over 10 years was also greater in Alzheimer disease than non-Alzheimer disease control subjects (P < 0.01). Islet amyloid was more frequent (P < 0.05) and extensive (P < 0.05) in patients with Alzheimer disease than in non-Alzheimer disease control subjects. However, diffuse and neuritic plaques were not more common in type 2 diabetes than in control subjects. In cases of type 2 diabetes when they were present, the duration of type 2 diabetes correlated with the density of diffuse (P < 0.001) and neuritic plaques (P < 0.01). In this community cohort from southeast Minnesota, type 2 diabetes and IFG are more common in patients with Alzheimer disease than in control subjects, as is the pathological hallmark of type 2 diabetes, islet amyloid. However, there was no increase in brain plaque formation in cases of type 2 diabetes, although when it was present, it correlated in extent with duration of diabetes. These data support the hypothesis that patients with Alzheimer disease are more vulnerable to type 2 diabetes and the possibility of linkage between the processes responsible for loss of brain cells and beta-cells in these diseases.

[ ] Re: Alzheimer's a form of diabetes?

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. >> 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]

I would guess it does:

The Lancet NeurologyVolume 5 • Number 1 • January 2006Copyright © 2006

ReviewRisk of dementia in diabetes mellitus: a systematic review

Although the association between diabetes and these modest changes in cognition is now well established, the relation between diabetes and dementia is an area of controversy. Early studies that reported a low rate of diabetes in patients with Alzheimer's disease,8, 9, 10 suggested that diabetes and Alzheimer's disease might not coexist.9 However, a more recent study suggested that type 2 diabetes or impaired fasting glucose might be present in up to 80% of patients with Alzheimer's disease.11

11 Janson J, Laedtke T, Parisi JE, O'Brien P, sen RC, PC, Increased risk of type 2 diabetes in Alzheimer disease . Diabetes (2004) 53 : pp 474-481 .

Increased risk of type 2 diabetes in Alzheimer disease.Janson J - Diabetes - 01-FEB-2004; 53(2): 474-81From NIH/NLM MEDLINE

NLM Citation ID:14747300 (PubMed)

Full Source Title:Diabetes

Author Affiliation:Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota, USA.

Authors:Janson J; Laedtke T; Parisi JE; O'Brien P; sen RC; PC

Abstract:Alzheimer disease and type 2 diabetes are characterized by increased prevalence with aging, a genetic predisposition, and comparable pathological features in the islet and brain (amyloid derived from amyloid beta protein in the brain in Alzheimer disease and islet amyloid derived from islet amyloid polypeptide in the pancreas in type 2 diabetes). Evidence is growing to link precursors of amyloid deposition in the brain and pancreas with the pathogenesis of Alzheimer disease and type 2 diabetes, respectively. Given these similarities, we questioned whether there may be a common underlying mechanism predisposing to islet and cerebral amyloid. To address this, we first examined the prevalence of type 2 diabetes in a community-based controlled study, the Mayo Clinic Alzheimer Disease Patient Registry (ADPR), which follows patients with Alzheimer disease versus control subjects without Alzheimer disease. In addition to this clinical study, we performed a pathological study of autopsy cases from this same community to determine whether there is an increased prevalence of islet amyloid in patients with Alzheimer disease and increased prevalence of cerebral amyloid in patients with type 2 diabetes. Patients who were enrolled in the ADPR (Alzheimer disease n = 100, non-Alzheimer disease control subjects n = 138) were classified according to fasting glucose concentration (FPG) as nondiabetic (FPG <110 mg/dl), impaired fasting glucose (IFG, FPG 110-125 mg/dl), and type 2 diabetes (FPG >126 mg/dl). The mean slope of FPG over 10 years in each case was also compared between Alzheimer disease and non-Alzheimer disease control subjects. Pancreas and brain were examined from autopsy specimens obtained from 105 humans (first, 28 cases of Alzheimer disease disease vs. 21 non-Alzheimer disease control subjects and, second, 35 subjects with type 2 diabetes vs. 21 non-type 2 diabetes control subjects) for the presence of islet and brain amyloid. Both type 2 diabetes (35% vs. 18%; P < 0.05) and IFG (46% vs. 24%; P < 0.01) were more prevalent in Alzheimer disease versus non-Alzheimer disease control subjects, so 81% of cases of Alzheimer disease had either type 2 diabetes or IFG. The slope of increase of FPG with age over 10 years was also greater in Alzheimer disease than non-Alzheimer disease control subjects (P < 0.01). Islet amyloid was more frequent (P < 0.05) and extensive (P < 0.05) in patients with Alzheimer disease than in non-Alzheimer disease control subjects. However, diffuse and neuritic plaques were not more common in type 2 diabetes than in control subjects. In cases of type 2 diabetes when they were present, the duration of type 2 diabetes correlated with the density of diffuse (P < 0.001) and neuritic plaques (P < 0.01). In this community cohort from southeast Minnesota, type 2 diabetes and IFG are more common in patients with Alzheimer disease than in control subjects, as is the pathological hallmark of type 2 diabetes, islet amyloid. However, there was no increase in brain plaque formation in cases of type 2 diabetes, although when it was present, it correlated in extent with duration of diabetes. These data support the hypothesis that patients with Alzheimer disease are more vulnerable to type 2 diabetes and the possibility of linkage between the processes responsible for loss of brain cells and beta-cells in these diseases.

[ ] Re: Alzheimer's a form of diabetes?

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. >> 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]

Perhaps they don't live long enough?

JR

Rodney wrote:

> 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.

>

>

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

>> article he cited.

>>

>> Mike

>>

>

>

>

>

[Guest guest]

Perhaps they don't live long enough?

JR

Rodney wrote:

> 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.

>

>

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

>> article he cited.

>>

>> Mike

>>

>

>

>

>