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Cell Cycle Activation and Aneuploid Neurons in Alzheimer's Disease | Molecular Neurobiology
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Molecular Neurobiology - Alzheimer
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Keywords {🔍}
google, scholar, cas, article, pubmed, disease, brain, alzheimers, cell, dna, human, neurons, chromosome, aneuploidy, neuronal, arendt, content, genet, cells, res, neurosci, cortex, med, cycle, expression, development, purkinje, alzheimer, neurol, rat, death, chromosomal, acta, yang, analysis, increased, neuropathol, biol, chun, yurov, iourov, vorsanova, cerebral, cerebellum, molecular, normal, pnas, science, mol, histochem,
Topics {✒️}
cytophotometrische dns-messungen month download article/chapter van der ploeg cell cycle-related proteins biulleten’ eksperimental’noĭ biologii fast-green histone estimations alpha-synuclein locus triplication linking cell-cycle dysfunction wave-length-scanning method childhood-onset psychotic disorders post-natal dna synthesis genome-wide phylogenetic analysis cell cycle activation chromosome segregation defects neuronal cell death selective neuronal vulnerability age-related neurodegenerative disorders full article pdf cell cycle regulation cell cycle regulators selective cell death privacy choices/manage cookies de la hera amyloid-ß peptide progenitor cell division cell cycle markers cell-cycle mechanisms low-level chromosomal aneuploidy neuronal differentiation control mammalian neuronal cells inversely recapitulates ontogenetic central nervous system measure chromosome instability european economic area mountcastle vb article arendt separate progenitor cells cell division markers oval cell proliferation individual cell nuclei kolichestvo kletok purkin iadrakh kletok purkin cell-cycle kinetics genome sequencing reveals neuronal nuclei polyploid chronic neurodegenerative disorder purkinje cell nuclei] induced gene expression critical molecular events premature centromere division
Questions {❓}
- Bernocchi G, Redi CA, Scherini E (1979) Feulgen-DNA content of the Purkinje neuron: “diploid” or “tetraploid”?
- Bregnard A, Knüsel A, Kuenzle CC (1975) Are all the neuronal nuclei polyploid?
- Herrup K, Yang Y (2007) Cell cycle regulation in the postmitotic neuron: oxymoron or new biology?
- Swartz FJ, Bhatnagar KP (1981) Are CNS neurons polyploid?
- Vincent I, Rosado M, Davies P (1996) Mitotic mechanisms in Alzheimer's disease?
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headline:Cell Cycle Activation and Aneuploid Neurons in Alzheimer's Disease
description:Alzheimer's disease (AD) is a chronic neurodegenerative disorder, characterized by synaptic degeneration associated with fibrillar aggregates of the amyloid-ß peptide and the microtubule-associated protein tau. The progression of neurofibrillary degeneration throughout the brain during AD follows a predictive pattern which provides the basis for the neuropathological staging of the disease. This pattern of selective neuronal vulnerability against neurofibrillary degeneration matches the regional degree of neuronal plasticity and inversely recapitulates ontogenetic and phylogenetic brain development which links neurodegenerative cell death to neuroplasticity and brain development. Here, we summarize recent evidence for a loss of neuronal differentiation control as a critical pathogenetic event in AD, associated with a reactivation of the cell cycle and a partial or full replication of DNA giving rise to neurons with a content of DNA above the diploid level. Neurons with an aneuploid set of chromosomes are also present at a low frequency in the normal brain where they appear to be well tolerated. In AD, however, where the number of aneuploid neurons is highly increased, a rather selective cell death of neurons with this chromosomal aberrancy occurs. This finding add aneuploidy to the list of critical molecular events that are shared between neurodegeneration and oncogenesis. It defines a molecular signature for neuronal vulnerability and directs our attention to a failure of neuronal differentiation control as a critical pathogenetic event and potential therapeutic target in AD.
datePublished:2012-04-13T00:00:00Z
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Apoptosis
Brain development
Cell death
Chromosome segregation
DNA replication
Neuronal vulnerability
Neurosciences
Neurobiology
Cell Biology
Neurology
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description:Alzheimer's disease (AD) is a chronic neurodegenerative disorder, characterized by synaptic degeneration associated with fibrillar aggregates of the amyloid-ß peptide and the microtubule-associated protein tau. The progression of neurofibrillary degeneration throughout the brain during AD follows a predictive pattern which provides the basis for the neuropathological staging of the disease. This pattern of selective neuronal vulnerability against neurofibrillary degeneration matches the regional degree of neuronal plasticity and inversely recapitulates ontogenetic and phylogenetic brain development which links neurodegenerative cell death to neuroplasticity and brain development. Here, we summarize recent evidence for a loss of neuronal differentiation control as a critical pathogenetic event in AD, associated with a reactivation of the cell cycle and a partial or full replication of DNA giving rise to neurons with a content of DNA above the diploid level. Neurons with an aneuploid set of chromosomes are also present at a low frequency in the normal brain where they appear to be well tolerated. In AD, however, where the number of aneuploid neurons is highly increased, a rather selective cell death of neurons with this chromosomal aberrancy occurs. This finding add aneuploidy to the list of critical molecular events that are shared between neurodegeneration and oncogenesis. It defines a molecular signature for neuronal vulnerability and directs our attention to a failure of neuronal differentiation control as a critical pathogenetic event and potential therapeutic target in AD.
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Brain development
Cell death
Chromosome segregation
DNA replication
Neuronal vulnerability
Neurosciences
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Cell Biology
Neurology
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