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Related Concept Videos

Alzheimer Disease l: Introduction01:29

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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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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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Updated: May 25, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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PP2A and Alzheimer disease.

L Torrent1, I Ferrer

  • 1Institut de Neuropatologia, Servei Anatomia Patològica, IDIBELL-Hospital Universitari de Bellvitge, Universitat de Barcelona, Hospitalet de LLobregat, Spain.

Current Alzheimer Research
|February 4, 2012
PubMed
Summary
This summary is machine-generated.

Protein phosphatase 2A (PP2A) dysfunction contributes to tau hyper-phosphorylation in Alzheimer disease (AD). Enhancing PP2A activity may offer a therapeutic strategy to reduce tau pathology in AD.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Microtubule-associated protein tau (tau) hyper-phosphorylation is a hallmark of Alzheimer disease (AD) and tauopathies.
  • Protein phosphatase 2A (PP2A) is a key enzyme responsible for dephosphorylating tau in the brain.
  • PP2A function is critical for maintaining neuronal health, and its dysfunction is implicated in AD pathogenesis.

Purpose of the Study:

  • To investigate the role of protein phosphatase 2A (PP2A) abnormalities in Alzheimer disease (AD).
  • To explore the potential of targeting PP2A as a therapeutic strategy for reducing tau hyper-phosphorylation in AD.

Main Methods:

  • Review and synthesis of existing literature on PP2A alterations in AD.
  • Analysis of reported changes in PP2A subunits, methylation, phosphorylation, and inhibitor levels in AD brains.
  • Evaluation of PP2A enzymatic activity in the context of AD pathology.

Main Results:

  • Multiple PP2A abnormalities are reported in AD, including altered subunit levels, reduced methylation, increased phosphorylation, and elevated inhibitor levels.
  • These alterations collectively lead to a loss of PP2A enzymatic activity in AD.
  • PP2A dysfunction is strongly associated with tau hyper-phosphorylation, a key event in AD.

Conclusions:

  • Protein phosphatase 2A (PP2A) is a critical regulator of tau phosphorylation and a potential therapeutic target in Alzheimer disease (AD).
  • Restoring or enhancing PP2A activity could mitigate tau hyper-phosphorylation and neurotoxicity in AD.
  • Further research is required to validate these findings and develop effective PP2A-based therapies for AD.