Perinuclear lamin a and nucleoplasmic lamin B2 characterize two types of hippocampal neurons through Alzheimer’s disease progression
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Background. Recent reports point to a nuclear origin of Alzheimer’s disease (AD). Aged postmitotic neurons try to repair their damaged DNA by entering the cell cycle. This aberrant cell cycle re-entry involves chromatin modifications where nuclear Tau and the nuclear lamin are involved. The purpose of this work was to elucidate their participation in the nuclear pathological transformation of neurons at early AD. Methodology. The study was performed in hippocampal paraffin embedded sections of adult, senile, and AD brains at I-VI Braak stages. We analyzed phospho-Tau, lamins A, B1, B2, and C, nucleophosmin (B23) and the epigenetic marker H4K20me3 by immunohistochemistry. Results. Two neuronal populations were found across AD stages, one is characterized by a significant increase of Lamin A expression, reinforced perinuclear Lamin B2, elevated expression of H4K20me3 and nuclear Tau loss, while neurons with nucleoplasmic Lamin B2 constitute a second population. Conclusions. The abnormal cell cycle reentry in early AD implies a fundamental neuronal transformation. This implies the reorganization of the nucleo-cytoskeleton through the expression of the highly regulated Lamin A, heterochromatin repression and building of toxic neuronal tangles. This work demonstrates that nuclear Tau and lamin modifications in hippocampal neurons are crucial events in age-related neurodegeneration. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
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Alzheimer’s disease; Cell-cycle; Heterochromatin; Hippocampus; Lamin A; Lamin B2; Neurofibrillary tangles; Tau protein lamin A; lamin B; lamin B1; lamin B2; lamin C; nucleophosmin; tau protein; unclassified drug; lamin A; lamin B; lamin B2; tau protein; adult; aged; Alzheimer disease; Article; brain nerve cell; cell cycle; cell population; cell transformation; cellular, subcellular and molecular biological phenomena and functions; controlled study; cytoskeleton; disease exacerbation; heterochromatin; heterochromatin repression; hippocampal CA1 region; hippocampal CA3 region; hippocampal neuron; human; human cell; human tissue; immunohistochemistry; neuronal tangle; protein depletion; protein expression; protein function; protein localization; protein modification; protein phosphorylation; Alzheimer disease; cell aging; cytology; disease exacerbation; genetics; hippocampus; metabolism; nerve cell; nuclear lamina; pathology; physiology; Alzheimer Disease; Cell Cycle; Cellular Senescence; Disease Progression; Hippocampus; Humans; Lamin Type A; Lamin Type B; Neurons; Nuclear Lamina; tau Proteins
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