Abstract
Cellular senescence contributes to Alzheimer's disease (AD) pathogenesis. Treatments that remove senescent cells, senolytics, improve brain outcomes in AD mice with amyloid-β or tau deposition. 3xTgAD mice develop both AD neuropathologies; however, Ng et al. report low p16INK4a-associated senescence in the brain. Senolytic treatment by genetic removal; dasatinib with quercetin (D+Q), which enter the brain; and ABT-263 with limited brain penetrance all reduced AD neuropathology. Refined measures of senescence and brain exposure would help clarify the benefits of senolytics despite low p16INK4a-associated senescence and potential limited brain penetrance.
| Original language | English |
|---|---|
| Pages (from-to) | 411-415 |
| Number of pages | 5 |
| Journal | Journal of Alzheimer's Disease |
| Volume | 98 |
| Issue number | 2 |
| DOIs | |
| State | Published - Mar 19 2024 |
Keywords
- Alzheimer's disease
- amyloid
- blood-brain barrier
- brain
- cellular senescence
- D+Q
- geroscience
- senolytics
- tau
- transgenic mice