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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
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Neuronal cell cycle re-entry mediates Alzheimer disease-type changes.

Andrew McShea1, Hyoung-gon Lee, Robert B Petersen

  • 1Department of Biology, CombiMatrix Corp, Mukilteo, WA 98275, USA.

Biochimica Et Biophysica Acta
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Alzheimer disease may stem from neurons inappropriately entering the cell cycle, similar to cancer. This study shows inducing cell cycle re-entry in neurons causes Alzheimer-like changes, offering a new therapeutic target.

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09:27

Cell Sorting of Neural Stem and Progenitor Cells from the Adult Mouse Subventricular Zone and Live-imaging of their Cell Cycle Dynamics

Published on: September 14, 2015

Area of Science:

  • Neuroscience
  • Cell Biology
  • Oncology

Background:

  • Alzheimer disease (AD) is linked to cell cycle-related protein re-expression in neurons.
  • This suggests neurodegeneration might share mechanisms with cancer, specifically cell cycle control.
  • Neurons are typically postmitotic and quiescent.

Purpose of the Study:

  • To test the hypothesis that neurodegeneration is a disease of inappropriate cell cycle control.
  • To investigate if inducing cell cycle re-entry in neurons leads to AD-like pathology.
  • To establish a neuronal cell model for studying AD.

Main Methods:

  • Adenoviral-mediated expression of c-myc and ras oncogenes.
  • Induction of cell cycle re-entry in primary cortical neurons.
  • Assessment of DNA content (BrdU, DAPI) and cyclin B1 re-expression.
  • Analysis of tau phosphorylation and conformational changes.

Main Results:

  • Postmitotic neurons were successfully driven into the cell cycle.
  • Cell cycle re-entry was confirmed by increased DNA content and cyclin B1 expression.
  • Neuronal cell cycle re-entry induced tau phosphorylation and conformational changes characteristic of AD.

Conclusions:

  • The cell cycle can be initiated in quiescent neurons.
  • This induced cell cycle re-entry results in a phenotype mirroring key features of Alzheimer disease neurodegeneration.
  • The developed neuronal cell model is valuable for exploring novel therapeutic strategies for AD.