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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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Journal ArticleDOI

Distinguishing adaptive plasticity from vulnerability in the aging hippocampus.

TL;DR: It is suggested that a reformulation of how normal aging could be understood from an adaptive perspective will lead to a deeper understanding of the secrets behind successful brain aging and recent cultural successes in facilitating these processes.
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Galectin-1 promotes basal and kainate-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus

TL;DR: The expression of galectin-1 was remarkably increased in activated astrocytes of the CA3 subregion and dentate gyrus of the hippocampus, and in nestin-positive neural progenitors in the dentate Gyrus, and it was concluded that galectIn-1 promotes basal and kainate-induced proliferation of Neural progenitor in the hippocampus.
Journal ArticleDOI

Localization of β-secretase memapsin 2 in the brain of Alzheimer's patients and normal aged controls

TL;DR: The expression of a newly identified beta-secretase, memapsin 2 (M2) or beta-site APP cleaving enzyme in deparaffinized sections from 10 AD patients and 10 aged matched controls and in frozen samples of parietal cortex revealed that senile plaques are not directly associated with the soma of M2-expressing neurons.
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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