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Journal ArticleDOI

Life and Death of Neurons in the Aging Brain

John H. Morrison, +1 more
- 17 Oct 1997 - 
- Vol. 278, Iss: 5337, pp 412-419
TLDR
The qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored.
Abstract
Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.

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Book

Concepts of Alzheimer Disease: Biological, Clinical, and Cultural Perspectives

TL;DR: Essays examine not only the prominent role that biomedical and clinical researchers have played in defining Alzheimer disease, but also the ways in which the perspectives of patients, their caregivers, and the broader public have shaped concepts.
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Age-related reduction in dopamine D1 receptors in the human brain: from late childhood to adulthood, a positron emission tomography study.

TL;DR: The present PET-study provides new evidence on the development of D1DR in humans in vivo which is of critical importance for understanding of the biology of neurodevelopmental disorders.
Journal ArticleDOI

Stereological quantification of GAD-67-immunoreactive neurons and boutons in the hippocampus of middle-aged and old Fischer 344 x Brown Norway rats.

TL;DR: Interestingly, GAD‐IR boutons did not show a decline in CA1, CA3, or dentate gyrus between middle and old age, and it is possible that loss of CA1 inhibitory interneurons in the dorsal hippocampus contributes to the learning and memory impairments reported in old rats.
References
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Journal ArticleDOI

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Heiko Braak, +1 more
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Journal ArticleDOI

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TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
Journal ArticleDOI

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TL;DR: The after‐effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro‐electrodes in rabbits anaesthetized with urethane.
Journal ArticleDOI

A new clinical scale for the staging of dementia.

TL;DR: The Clinical Dementia Rating (CRD) was developed for a prospective study of mild senile dementia—Alzheimer type (SDAT), and was found to distinguish unambiguously among older subjects with a wide range of cognitive function.
Journal ArticleDOI

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD): Part II. Standardization of the neuropathologic assessment of Alzheimer's disease

TL;DR: The Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed a practical and standardized neuropathology protocol for the postmortem assessment of dementia and control subjects, which provides neuropathologic definitions of such terms as “definite Alzheimer's disease” (AD), “probable AD,” “possible AD” and “normal brain” to indicate levels of diagnostic certainty.
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