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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

Reactive oxygen species, dietary restriction and neurotrophic factors in age-related loss of myenteric neurons

TL;DR: It is hypothesized that CR enhances antioxidant defence through neurotrophic factor signalling, thereby reducing age‐related increases in neuronal ROS levels and in ROS‐induced cell death, and protects age‐matched neurons against ROS‐ induced apoptosis.
Journal ArticleDOI

Neuronal and morphological bases of cognitive decline in aged rhesus monkeys

TL;DR: Age-related changes in anatomical, neuronal, and synaptic parameters within brain areas implicated in cognition and whether these changes are associated with cognitive decline are summarized.
Journal ArticleDOI

Conservation of neuron number and size in entorhinal cortex layers II, III, and V/VI of aged primates

TL;DR: A lack of morphologically evident neurodegeneration in primate entorhinal cortex with aging further supports the concept that fundamental differences exist between the processes of normal “healthy” aging and pathologic age‐related neurodegnerative disorders such as Alzheimer's disease.
Journal ArticleDOI

The neuropathology of schizophrenia: A selective review of past studies and emerging themes in brain structure and cytoarchitecture.

TL;DR: The evidence converges on a progressive neurodevelopmental model of schizophrenia related to altered neuroplasticity, which supports a particular vulnerability of inhibitory cortical circuits with markers of interneurons showing some of the more consistent reductions in schizophrenia.
Journal ArticleDOI

Nuclear DNA damage as a direct cause of aging.

TL;DR: Evidence that damage to nuclear DNA (nDNA) is a direct cause of aging in addition to the effects of nDNA damage on cancer, apoptosis, and cellular senescence is presented.
References
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Journal ArticleDOI

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Heiko Braak, +1 more
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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

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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