Journal ArticleDOI
Life and Death of Neurons in the Aging Brain
John H. Morrison,Patrick R. Hof +1 more
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.read more
Citations
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Dynamic mapping of human cortical development during childhood through early adulthood
Nitin Gogtay,Jay N. Giedd,Leslie Lusk,Kiralee M. Hayashi,Deanna Greenstein,A. Catherine Vaituzis,Tom F. Nugent,David H. Herman,Liv S. Clasen,Arthur W. Toga,Judith L. Rapoport,Paul M. Thompson +11 more
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.
Journal ArticleDOI
A specific amyloid-|[beta]| protein assembly in the brain impairs memory
Sylvain Lesné,Ming Teng Koh,Linda Kotilinek,Rakez Kayed,Charles G. Glabe,Austin J. Yang,Michela Gallagher,Karen H. Ashe +7 more
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.
Journal ArticleDOI
Mapping cortical change across the human life span
Elizabeth R. Sowell,Bradley S. Peterson,Paul M. Thompson,Suzanne E. Welcome,Amy L. Henkenius,Arthur W. Toga +5 more
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
David H. Salat,Randy L. Buckner,Randy L. Buckner,Abraham Z. Snyder,Douglas N. Greve,Rahul S. Desikan,Evelina Busa,John C. Morris,Anders M. Dale,Bruce Fischl +9 more
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.
Journal ArticleDOI
Neural plasticity in the ageing brain
Sara N. Burke,Carol A. Barnes +1 more
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
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Patrick R. Hof,Esther A. Nimchinsky,Marco R. Celio,Constantin Bouras,Constantin Bouras,John H. Morrison +5 more
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.
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Journal ArticleDOI
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