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Tau and neuron aging.

Jesus Avila1, Elena Gomez de Barreda, Noemi Pallas-Bazarra

  • 1Centro de Biología Molecular Severo Ochoa, CSIC-UAM, 28049 Madrid, Spain. ; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain.

Aging and Disease
|February 21, 2013
PubMed
Summary
This summary is machine-generated.

Changes in tau protein isoforms, due to splicing or modifications, impact neuron function in aging and disease. Altered tau can cause toxic gain of function or loss of function, affecting aging mammals.

Keywords:
Alzheimer diseaseTau isoformsposttranslational modifications

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Published on: January 2, 2015

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Tau protein exists as multiple isoforms generated through alternative splicing and post-translational modifications.
  • The expression levels of tau isoforms vary across different neurons during development, aging, and in disease states like tauopathies.
  • Modified tau, through phosphorylation or aggregation, can lead to a toxic gain of function, particularly observed in aging organisms.

Purpose of the Study:

  • To discuss the functional implications of different tau protein isoforms and their modifications.
  • To explore the consequences of altered tau protein function, including both gain and loss of function, in aging and disease.
  • To highlight the role of tau protein in age-related neurological conditions and potential iron toxicity.

Main Methods:

  • Review and synthesis of existing literature on tau protein biology, alternative splicing, and post-translational modifications.
  • Analysis of phenotypic changes associated with altered tau protein levels and functions in mammalian models.
  • Discussion of the link between tau protein dysfunction, aging, and specific pathologies such as tauopathies and iron toxicity.

Main Results:

  • Tau protein isoforms are dynamically regulated and their altered proportions are implicated in neuronal aging and tauopathies.
  • Gain of toxic function in modified tau (phosphorylated or aggregated) contributes to disease phenotypes, especially in aging.
  • Loss of tau function can lead to detrimental effects, including iron toxicity, in aging animals lacking functional tau.

Conclusions:

  • The dynamic nature of tau protein isoforms and their modifications plays a critical role in neuronal health and disease.
  • Both gain and loss of tau protein function have significant consequences, particularly during the aging process.
  • Understanding tau protein regulation and dysfunction is crucial for addressing age-related neurological disorders and tauopathies.