In order to determine whether cortical fibrous astrocytes increase with age, we studied 25 patients ranging in age from 24 to 100 years with no clinical or pathological evidence of dementia or other cerebral disorder. Paraffin sections of mid-frontal cortex were obtained and stained with the avidin-biotin immunolabeling procedure for glial intermediate filament protein. The resulting immunolabeled fibrous astrocytes were then counted in the molecular and cellular (cortical laminae 2-6) layers. Populations of fibrous astrocytes in both layers varied widely among individuals, and in the molecular layer their numbers were not significantly correlated with advancing age. In the cellular layer, however, despite widely ranging cell counts among individuals within the same decades of life, there was a significant linear increase with age. Our data suggest that the increase occurs or accelerates significantly after age 70, but the case numbers preclude reaching such a conclusion with statistical confidence. However, when the patients are divided into those less than 70 and those older, fibrous astrocytes in the cellular layer are shown to be significantly increased in the latter group compared to the former.

Adult↗

PubMedDate not supplied

Accumulation of amyloid precursor fragment in Alzheimer plaques.

Regenerative and degenerative neurites are components of classical senile plaques found in brain tissue of patients with Alzheimer's disease (AD). Amyloid beta/A4-protein derived from its precursor, amyloid beta/A4-protein precursor (APP/ABPP), constitutes the major portion of the amyloid core of senile plaques. A large N-terminal portion of APP (approximately Mr 100,000) is released from cells, leaving a minor C-terminal portion (approximately Mr 15,000) behind. A series of antisera against various sequences of APP were prepared and used to study the localization of each sequence in brain tissue. Plaque neurites stained as intensely as neuronal cell bodies with three antisera against the N-terminal portion of APP (N-terminal to a.a. 225), whereas five other antisera directed against the other C-terminal portions of APP (a.a. 284 to C-terminal) and antisera against the Kunitz-type protease inhibitor portion of APP stained plaque neurites less intensely than neuronal cell bodies in the hippocampus. These results suggest that a major part of the APP present in the neuritic component of senile plaques is a fragment representing the N-terminal one-third of the molecule.

Aged↗

PubMedDate not supplied

Microscopic pattern of healing of the cryogenic thalamic lesion.

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Autopsy↗

PubMedDate not supplied

Commentary. Copernicus revisited: amyloid beta in alzheimer disease.

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Alzheimer Disease↗

PubMedDate not supplied

Life span and synapses: will there be a primary senile dementia?

In the course of normal aging from about age 20 to 100, the population density of neocortical synapses declines toward, but not reaching, the level found in Alzheimer disease. A deficiency of synapses at birth or due to inadequate childhood education would theoretically cause the synaptic slope to reach the Alzheimer level early. The normal slope would cross into that dementia range at about age 130, resulting in true primary senile dementia without regard to the presence of plaques and tangles.

Adolescent↗

PubMedDate not supplied

Position paper on diagnostic criteria for Alzheimer disease.

The lesions of Alzheimer disease (AD) consist of synapse and neuron loss associated with progressive deposition of amyloid as diffuse and neuritic plaques and accumulating tau abnormalities in the form of neurofibrillary tangles and neuropil threads. Diagnostic criteria for Alzheimer disease constitute arbitrary cut-off levels above which AD is deemed to exist, and below which lesser amounts of the same abnormalities are relegated to the nebulous category of aging changes. Demanding neocortical tangles for a diagnosis of AD sacrifices sensitivity on the altar of specificity, since, while such lesions usually represent an advanced stage in the orderly evolution of AD, lighter burdens of plaque-predominant AD pathology with tangles confined to the medial temporal lobe can cause dementia when associated with concomitant synapse loss. Such muted AD pathology typifies the Lewy body variant of AD, and it serves to segregate it from pure Lewy body disease. We endorse the semiquantitative neuritic-plaque based criteria from CERAD for routine diagnosis, and Braak staging with descriptive profiling of AD lesions in a research context.

Aged↗

PubMedDate not supplied

Immunoelectron microscopy of Alzheimer and Pick brain tissue labelled with the monoclonal antibody Alz-50.

Previous studies have shown that Alzheimer and Pick brains contain abnormally elevated amounts of a 68 Kd protein detected by the monoclonal antibody Alz-50. We have used immunoperoxidase and immunological techniques to localize Alz-50-reactive epitopes in sections from Alzheimer and Pick brains at the ultrastructural level. Detectable immunoreactivity was restricted to the paired helical filaments of Alzheimer neurofibrillary tangles and to the paired helical and straight filaments of Pick bodies. In Alzheimer tissue, the antibody also labelled scattered neuronal paired helical filaments that were not aggregated into neurofibrillary tangles. Amorphous components of Pick bodies and other constituents in the Alzheimer and Pick brain tissue were not immunostained.

Aged↗

PubMedDate not supplied

Quantitative assessment of dietary adherence in patients with insulin-dependent diabetes mellitus.

Research on the education of diabetic patients in diet management suffers from lack of an adequate method for describing patients' dietary behavior. In this report, a method is proposed for the quantitative assessment of dietary adherence in patients with IDDM. The method relies on comparisons between individualized diet plans and actual consumption as reflected by 24-h diet recalls. Data are presented that suggest this method has reliability and validity. In a sample of 97 patients with IDDM, nearly two-thirds adhered to the number and timing of planned feedings, while only about 10% of patients adhered to planned exchanges, 90% of the time. The average patient added or deleted one exchange for every four exchanges in the diet plan.

Adolescent↗