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Newest in this topic

  1. Alzheimer's disease-associated R47H TREM2 increases, but wild-type TREM2 decreases, microglial phagocytosis of synaptosomes and neuronal loss 2022-12-08
  2. Evaluation of the Expression of Amyloid Precursor Protein and the Ratio of Secreted Amyloid Beta 42 to Amyloid Beta 40 in SH-SY5Y Cells Stably Transfected with Wild-Type, Single-Mutant and Double-Mutant Forms of the APP Gene for the Study of Alzheimer's Disease Pathology 2017-04-17
  3. Tau post-translational modifications in wild-type and human amyloid precursor protein transgenic mice 2015-07-20

Studies

4 studies carry this tag.

Date range

2012 to 2022

Top journals

  • Applied biochemistry and biotechnology 1
  • FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1
  • Glia 1
  • Nature 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. Alzheimer's disease-associated R47H TREM2 increases, but wild-type TREM2 decreases, microglial phagocytosis of synaptosomes and neuronal loss

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Glia 2022-12-08 TREM2 and immune genetics

    Triggering receptor on myeloid cells 2 (TREM2) is an innate immune receptor, upregulated on the surface of microglia associated with amyloid plaques in Alzheimer's disease (AD).

  2. Neuroblastoma cell lines such as SH-SY5Y are the most frequently utilized models in neurodegenerative research, and their use has advanced the understanding of the pathology of neurodegeneration over the past few decades.

  3. Tau post-translational modifications in wild-type and human amyloid precursor protein transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Nature neuroscience 2015-07-20 Risk genes beyond APOE

    The microtubule-associated protein tau has been implicated in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders.

  4. The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2012-03-29 Biomarkers

    Genetically engineered mice have been generated to model cerebral β-amyloidosis, one of the hallmarks of Alzheimer disease (AD) pathology, based on the overexpression of a mutated cDNA of the amyloid-β precursor protein (AβPP) or by knock-in of the murine Aβpp gene alone or with presenilin1 mutations.

All topic tags with their study counts