Document
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Continuant
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Review
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RDF description of Aging and Alzheimer's disease connection: Nuclear Tau and lamin A - http://orbis.uaslp.mx/vivo/individual/scopus9609
rights: termsOfUse
date: 2026-08-24T21:45:46
publisher: vivo
type: Document

Article
type: Class

Aging and Alzheimer's disease connection: Nuclear Tau and lamin A
type: Information Content Entity
type: Entity
crisid: 9610
doi: 10.1016/j.neulet.2021.135741
type: Review
related by: authorship_66788
type: Document
related by: authorship_66787
most specific type: Document
type: Thing
e iscopus: 2-s2.0-85101533986
pmid: 33610669
chemicalscas: MAPT protein, human; tau Proteins
related by: authorship_66789
artnum: 135741
abstract: Age-related pathologies like Alzheimer‘s disease (AD) imply cellular responses directed towards repairing DNA damage. Postmitotic neurons show progressive accumulation of oxidized DNA during decades of brain aging, which is especially remarkable in AD brains. The characteristic cytoskeletal pathology of AD neurons is brought about by the progressive changes that neurons undergo throughout aging, and their irreversible nuclear transformation initiates the disease. This review focusses on critical molecular events leading to the loss of plasticity that underlies cognitive deficits in AD. During healthy neuronal aging, nuclear Tau participates in the regulation of the structure and function of the chromatin. The aberrant cell cycle reentry initiated for DNA repair triggers a cascade of events leading to the dysfunctional AD neuron, whereby Tau protein exits the nucleus leading to chromatin disorganization. Lamin A, which is not typically expressed in neurons, appears at the transformation from senile to AD neurons and contributes to halting the consequences of cell cycle reentry and nuclear Tau exit, allowing the survival of the neuron. Nevertheless, this irreversible nuclear transformation alters the nucleic acid and protein synthesis machinery as well as the nuclear lamina and cytoskeleton structures, leading to neurofibrillary tangles formation and final neurodegeneration. © 2021 Elsevier B.V.
most specific type: Review
freetext keyword: Aging; Alzheimer's disease; Chromatin; Hippocampal neuron; Lamin A; Nuclear lamin; Tau protein lamin A; tau protein; MAPT protein, human; tau protein; aging; Alzheimer disease; cell cycle; cognitive defect; cytoskeleton; DNA damage; DNA repair; human; nerve cell plasticity; nerve degeneration; neurofibrillary tangle; nuclear lamina; nucleic acid synthesis; priority journal; protein expression; protein synthesis; Review; aging; Alzheimer disease; brain; metabolism; nerve cell; Aging; Alzheimer Disease; Brain; Humans; Neurons; tau Proteins
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type: Article
origen: scopus
type: Generically Dependent Continuant
date time value: review date 9610
estado: published
volume: 749
has publication venue: Neuroscience Letters

Information Content Entity
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Neuroscience Letters
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type: Collection
publication venue for: Aging and Alzheimer's disease connection: Nuclear Tau and lamin A
type: Document
type: Thing
type: Continuant
type: Periodical
type: Journal
type: Entity
type: Generically Dependent Continuant