Alzheimer's Disease, Down's Syndrome, and Aging: The Genetic Approach

Sinex, F. Marott; Myers, Richard H.

doi:10.1111/j.1749-6632.1982.tb26839.x

Cited by 39 publications

(12 citation statements)

References 7 publications

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“…Several authors have identified distinct stages associated with Alzheimer's disease. Mackey (1983) and Sinex and Myers (1982) have identified early stages that resemble each other. In these stages the person becomes less involved with events, objects, and people in the environment.…”

Section: Behavioral and Physical Description Of Sdatmentioning

confidence: 96%

“…Mackey (1983) separated the middle stage into two separate periods. Both Mackey (1983) and Sinex and Myers (1982) listed irritability, resentment, wandering, and further loss of communication as characteristic of this stage. Progressive deterioration may result in placement in an institution, according to Sinex and Myers.…”

Section: Behavioral and Physical Description Of Sdatmentioning

confidence: 99%

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Alzheimer's Disease: The Death of the Disease

McBroom

1986

Counseling and Values

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Alzheimer's disease, a form of dementia, affects middle‐age and older adults. The disease is becoming more evident because of growing numbers of older people and better diagnosis and detection methods. The author describes the behavioral and physical symptoms of the disease as well as specific suggestions for care of patients with Alzheimer's disease. Counselors can use this article to provide family members and other persons dealing with Alzheimer's disease with information and practical advice about dealing with the changes occurring in the patient.

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Section: Behavioral and Physical Description Of Sdatmentioning

confidence: 96%

Section: Behavioral and Physical Description Of Sdatmentioning

confidence: 99%

Alzheimer's Disease: The Death of the Disease

McBroom

1986

Counseling and Values

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“…Thus, any underlying genetic diathesis would probably become fully apparent only in extreme old age. Many relatives still under observation will not yet have reached such an age, and others will have died from competing causes before their genetic predisposition (if any) was expressed (Larsson et al, 1963;Sinex and Myers, 1982;Breitner et at., 1986a,b). Failure to consider or adjust for this possibility must result in underestimation of the familial predisposition to AD.…”

Section: Age-dependent Onsetmentioning

confidence: 99%

Handbook of Psychopharmacology

Iversen¹,

Iversen²,

Snyder³

1988

608

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“…In 1982, an extensive molecular biology research program was started to investigate the chromosomal alterations in AD and it reported identical chromosomal abnormalities in Down's syndrome and AD [3]. It was clearly ascertained that a point mutation at codon 717 in chromosome 21 is responsible for early onset forms of AD [4].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Genome Lesions in the Pathogenesis of Sporadic Alzheimer’s Disease

Meier‐Ruge¹,

Bertoni–Freddari²

1999

Gerontology

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Background: The recent, magnificent results of molecular biology concerning β-amyloid (βA) metabolism in early onset Alzheimer’s disease (AD) have generated a series of new findings and, in turn, a new etiological concept. Attention on the early events in the pathogenesis of AD has been shifted from the chromosomal abnormalities in the nucleus of nerve cells onto genetic changes in the mitochondrial genome. This offers a new pathogenetic approach which also opens new pharmacological challenges particularly for the episodic forms of AD. Objective: Alterations occurring at the mitochondrial genome result in major consequences of oxidative phosphorylation and, if a specific threshold is exceeded, they may constitute important causative events in the apoptosis of selected nerve cells. The fact that the main source of mitochondrial metabolism is its glucose turnover allows monitoring brain changes in glucose metabolism by 18F-2 deoxyglucose positron emission tomography. In the demented brain, a low glucose turnover causes a cholinergic deficit by decreasing the synthetic rate of acetyl coenzyme A (AcCoA). AcCoA represents the key substrate for the acetylation of choline to acetylcholine by choline acetyltransferase. The consistent energy need for AcCoA synthesis appears obvious when considering that 1 molecule of glucose generates just 2 molecules of AcCoA, but 38 molecules of ATP. In the brain, AcCoA is exclusively synthesized in the glycolitic pathway. Generation of βA is increased if the synthetic rate of ATP drops below a critical threshold: under these conditions, the βA precursor protein (βAPP) is inserted only in part into synaptic membranes which have the highest βAPP turnover. In conditions of short ATP supply, βAPP is not split at the β region by an ATP-activated protease and this results in a substantial increase in uncleaved βA molecules. Conclusion: Peroxidative alterations in mitochondrial DNA are of importance in degenerative diseases of postmitotic tissues, particularly in degenerative diseases. This offers a new pharmacological approach for the treatment of AD. Neurotrophic factors and estrogen seem to be the first pharmacological leads.

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Alzheimer's Disease, Down's Syndrome, and Aging: The Genetic Approach

Cited by 39 publications

References 7 publications

Alzheimer's Disease: The Death of the Disease

Alzheimer's Disease: The Death of the Disease

Handbook of Psychopharmacology

Mitochondrial Genome Lesions in the Pathogenesis of Sporadic Alzheimer’s Disease

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