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Aging and Alzheimer's disease connection: Nuclear Tau and lamin A
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.
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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