Home › Research › Topics › apoptosis
apoptosis
5 studies tagged apoptosis, dated 1997-06-01 to 2017-07-21. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Role of Caspase-3-Mediated Apoptosis in Chronic Caspase-3-Cleaved Tau Accumulation and Blood-Brain Barrier Damage in the Corpus Callosum after Traumatic Brain Injury in Rats 2017-07-21
- Blockade of 12-lipoxygenase expression protects cortical neurons from apoptosis induced by beta-amyloid peptide 2004-08-01
- Apoptosis of astrocytes with enhanced lysosomal activity and oligodendrocytes in white matter lesions in Alzheimer's disease 2002-06-01
Studies
5 studies carry this tag.
Date range
1997 to 2017
Top journals
- Brain research. Molecular brain research 1
- Cell death and differentiation 1
- Journal of neurotrauma 1
- Neuropathology and applied neurobiology 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.
-
Traumatic brain injury (TBI) may be a significant risk factor for development of neurodegenerative disorders such as chronic traumatic encephalopathy (CTE), post-traumatic epilepsy (PTE), and Alzheimer's (AD) and Parkinson's (PD) diseases.
-
The cyclo-oxygenase (COX) and lipoxygenase (LOX) pathways belong to the eicosanoid synthesis pathway, a major component of the chronic inflammatory process occurring in Alzheimer's disease (AD).
-
Glial changes are intimately associated with the white matter lesions, and regressive changes in astrocytes and loss of oligodendroglial cells have been reported.
-
The S100beta protein is overexpressed in the brain of patients with Alzheimer's disease and Down's syndrome and is able to induce apoptosis in neurons at high concentrations.
-
Most autosomal dominant inherited forms of early onset Alzheimer's disease (AD) are caused by mutations in the presenilin-1 (PS-1) gene on chromosome 14.