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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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Citations
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A neuronal morphologic type unique to humans and great apes

TL;DR: The existence and distribution of an unusual type of projection neuron, a large, spindle-shaped cell, in layer Vb of the anterior cingulate cortex of pongids and hominids is reported, which suggests some of the differential neuronal susceptibility that occurs in the human brain in the course of age-related dementing illnesses may have appeared only recently during primate evolution.
Journal ArticleDOI

Brain Glucose Hypometabolism and Oxidative Stress in Preclinical Alzheimer's Disease

TL;DR: Findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD are reviewed.
Journal ArticleDOI

Neuroplasticity Failure in Alzheimer's Disease: Bridging the Gap between Plaques and Tangles

TL;DR: This research examines the role of language impairment in the development of Alzheimer's disease and the role that language impairment plays in the progression of disease.
Journal ArticleDOI

fMRI studies of associative encoding in young and elderly controls and mild Alzheimer’s disease

TL;DR: The pattern of fMRI activation during the encoding of novel associations is differentially altered in the early stages of Alzheimer’s disease compared with normal aging.
References
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Journal ArticleDOI

Neuropathological stageing of Alzheimer-related changes.

Heiko Braak, +1 more
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
Journal ArticleDOI

A synaptic model of memory: long-term potentiation in the hippocampus

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.
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Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.

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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