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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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Dynamic mapping of human cortical development during childhood through early adulthood

TL;DR: The dynamic anatomical sequence of human cortical gray matter development between the age of 4-21 years using quantitative four-dimensional maps and time-lapse sequences reveals that higher-order association cortices mature only after lower-order somatosensory and visual cortices are developed.
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A specific amyloid-|[beta]| protein assembly in the brain impairs memory

TL;DR: It is found that memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-β assembly, which is proposed to be Aβ*56 (Aβ star 56), which may contribute to cognitive deficits associated with Alzheimer's disease.
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Mapping cortical change across the human life span

TL;DR: A significant, nonlinear decline in GMD with age is found over dorsal frontal and parietal association cortices on both the lateral and interhemispheric surfaces, indicating that the posterior temporal cortices have a more protracted course of maturation than any other cortical region.
Journal ArticleDOI

Thinning of the cerebral cortex in aging

TL;DR: It is demonstrated that cortical thinning occurs by middle age and spans widespread cortical regions that include primary as well as association cortex.
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Neural plasticity in the ageing brain

TL;DR: Major advances in understanding of age-related changes in the medial temporal lobe and prefrontal cortex are discussed and how these changes in functional plasticity contribute to behavioural impairments in the absence of significant pathology.
References
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Journal ArticleDOI

Recognition of tau epitopes by anti-neurofilament antibodies that bind to Alzheimer neurofibrillary tangles

TL;DR: Results suggest that staining of ANT by anti-NF antibodies may be due to cross-reaction of anti- NF with epitopes in tau proteins, the epitope in axons, NF, and tau are sensitive to the effect of phosphatase, whereas the majority of those in ANT are not, and some of the epitopesIn ANT that are shared with NF and t Tau are not readily accessible to antibody binding.
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A monoclonal antibody to non-phosphorylated neurofilament protein marks the vulnerable cortical neurons in Alzheimer's disease.

TL;DR: A monoclonal antibody to non-phosphorylated neurofilament protein labels a distinct subset of pyramidal cells in the normal human cortex which have a distribution very similar to that of neurofibrillary tangles in brains from patients with Alzheimer's disease.
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Calretinin-immunoreactive neocortical interneurons are unaffected in Alzheimer's disease.

TL;DR: The results support the notion that the pathological process in Alzheimer's disease involves specific cellular populations sharing particular morphological and neurochemical characteristics, and suggest that calretinin-immunoreactive neurons, like other calcium-binding protein-containing interneurons, are resistant to degeneration in Alzheimer't disease.
Journal Article

The significance of morphometric procedures in the investigation of age changes in cytoarchitectonic structures of human brain.

TL;DR: The investigations were performed on NISSL-stained cytoarchitectonic images of totally 78 human brains in the frontal area 11 (inside sulcus olfactorius) and in the visual cortex (area 17) with 60 samples and the main result is that every gray structure of the brain has its own history.
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Beta A4 deposits are constant in the brain of the oldest old: an immunocytochemical study of 20 French centenarians.

TL;DR: The constant deposition of beta A4 protein in the brain of very old people indicates that this process does not spare a large proportion of this population, and favorsbeta A4 accumulation in thebrain being an ineluctable age-related process.
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