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Home › Research › Topics › disruption

disruption

5 studies tagged disruption, dated 2001-11-01 to 2023-09-01. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration 2023-09-01
  2. Loss of Trem2 in microglia leads to widespread disruption of cell coexpression networks in mouse brain 2018-05-17
  3. Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating 2008-06-01

Studies

5 studies carry this tag.

Date range

2001 to 2023

Top journals

  • Neuron 2
  • Cell 1
  • Journal of neurochemistry 1
  • Neurobiology of aging 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. Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell 2023-09-01 Genetics

    Persistent DNA double-strand breaks (DSBs) in neurons are an early pathological hallmark of neurodegenerative diseases including Alzheimer's disease (AD), with the potential to disrupt genome integrity.

  2. Loss of Trem2 in microglia leads to widespread disruption of cell coexpression networks in mouse brain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2018-05-17 TREM2 and immune genetics

    Rare heterozygous coding variants in the triggering receptor expressed in myeloid cells 2 (TREM2) gene, conferring increased risk of developing late-onset Alzheimer's disease, have been identified.

  3. Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2008-06-01 Risk genes beyond APOE

    Mutations in presenilins (PS) are the major cause of familial Alzheimer's disease (FAD) and have been associated with calcium (Ca2+) signaling abnormalities.

  4. Disruption of neurogenesis by amyloid beta-peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2002-12-01 Risk genes beyond APOE

    Neurogenesis occurs in the adult mammalian brain and may play roles in learning and memory processes and recovery from injury, suggesting that abnormalities in neural progenitor cells (NPC) might contribute to the pathogenesis of disorders of learning and memory in humans.

  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.

All topic tags with their study counts