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Home › Research › Topics › axonal-transport

axonal-transport

6 studies tagged axonal-transport, dated 2000-11-01 to 2011-05-01. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy 2011-05-01
  2. Tau reduction prevents Abeta-induced defects in axonal transport 2010-09-09
  3. Axonal transport rates in vivo are unaffected by tau deletion or overexpression in mice 2008-02-01

Studies

6 studies carry this tag.

Date range

2000 to 2011

Top journals

  • Neuron 2
  • The Journal of neuroscience : the official journal of the Society for Neuroscience 2
  • Nature 1
  • Science (New York, N.Y.) 1

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2011-05-01 Risk genes beyond APOE

    In the hallmark neuritic dystrophy of Alzheimer's disease (AD), autophagic vacuoles containing incompletely digested proteins selectively accumulate in focal axonal swellings, reflecting defects in both axonal transport and autophagy.

  2. Tau reduction prevents Abeta-induced defects in axonal transport

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2010-09-09 Risk genes beyond APOE

    Amyloid-β (Aβ) peptides, derived from the amyloid precursor protein, and the microtubule-associated protein tau are key pathogenic factors in Alzheimer's disease (AD).

  3. Axonal transport rates in vivo are unaffected by tau deletion or overexpression in mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2008-02-01 Biomarkers

    Elevated tau expression has been proposed as a possible basis for impaired axonal transport in Alzheimer's disease.

  4. Kinesin-mediated axonal transport of a membrane compartment containing beta-secretase and presenilin-1 requires APP

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2001-12-01 Risk genes beyond APOE

    Proteolytic processing of amyloid precursor protein (APP) generates amyloid-beta peptide and has been implicated in the pathogenesis of Alzheimer's disease.

  5. Disruption of axonal transport and neuronal viability by amyloid precursor protein mutations in Drosophila

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2001-11-01 Risk genes beyond APOE

    We tested the hypothesis that amyloid precursor protein (APP) and its relatives function as vesicular receptor proteins for kinesin-I. Deletion of the Drosophila APP-like gene (Appl) or overexpression of human APP695 or APPL constructs caused axonal transport phenotypes similar to kinesin and dynein mutants.

  6. Axonal transport of amyloid precursor protein is mediated by direct binding to the kinesin light chain subunit of kinesin-I

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2000-11-01 Risk genes beyond APOE

    We analyzed the mechanism of axonal transport of the amyloid precursor protein (APP), which plays a major role in the development of Alzheimer's disease.

All topic tags with their study counts