After a tough year, during which believers in immunotherapy for Alzheimer’s disease have had to fend off vociferous criticism, the news now appears to pick up...
On Saturday, 27 October, in Los Angeles, an unusual conference marked a paradigm shift in the Alzheimer disease movement...
Flurizan has floundered in an 18-month Phase 3 clinical trial in patients with mild Alzheimer disease...
A new study finds that the cancer drug imatinib does not lower Aβ in humans, casting doubt on a previously described relationship between imatinib, γ-secretase activating protein (GSAP), and Aβ.
Two new papers rekindle acrimonious debate about exactly what “loss-of-function” means when it comes to presenilin mutations in Alzheimer’s pathogenesis.
Presenilin 2 resides almost exclusively in late endosomes, multivesicular bodies, and lysosomes, where it generates a pool of aggregation-prone Aβ. Some PS-1 mutations phenocopy this intraneuronal distribution.
The EPOCH trial of verubecestat was halted for lack of efficacy. APECS trial in prodromal AD continues.
Researchers claim this failed drug allows Aβ to accumulate inside cells, while small peptides cleaved from the C-terminal end of APP become trapped in membranes.
Aging lymphatic vessels in the meninges hinder waste clearance from the brain and exacerbate Aβ build-up.
In the future, could Alzheimer disease treatments come as an ointment, or a skin patch?...
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
Recent studies have identified rare loss-of-function variants that cause Alzheimer’s with nearly 100 percent penetrance. Now there are 17 more.
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?