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Newest in this topic

  1. TREM2 splice isoforms generate soluble TREM2 species that disrupt long-term potentiation 2023-02-20
  2. APOE4 disrupts intracellular lipid homeostasis in human iPSC-derived glia 2021-03-01
  3. Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy 2011-05-01

Studies

4 studies carry this tag.

Date range

2006 to 2023

Top journals

  • Genome medicine 1
  • Neuron 1
  • Science translational medicine 1
  • The Journal of neuroscience : the official journal of the Society for Neuroscience 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. TREM2 splice isoforms generate soluble TREM2 species that disrupt long-term potentiation

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Genome medicine 2023-02-20 TREM2 and immune genetics

    TREM2 transcripts can give rise to a heterogeneous pool of sTREM2 which acts to inhibit LTP.

  2. APOE4 disrupts intracellular lipid homeostasis in human iPSC-derived glia

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Science translational medicine 2021-03-01 Genetics

    The E4 allele of the apolipoprotein E gene ( APOE ) has been established as a genetic risk factor for many diseases including cardiovascular diseases and Alzheimer's disease (AD), yet its mechanism of action remains poorly understood.

  3. 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.

  4. Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2006-07-01 Risk genes beyond APOE

    Degeneration of basal forebrain cholinergic neurons (BFCNs) contributes to cognitive dysfunction in Alzheimer's disease (AD) and Down's syndrome (DS).

All topic tags with their study counts