Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
Carriers of a rare hypomorphic gene variant develop a frontotemporal dementia that features Alzheimer’s-like neurofibrillary tangles.
Expert panel concludes there’s little risk based on current evidence.
The R1279Q variant of angiotensin-converting enzyme associates with AD and causes neurodegeneration in mice. In a model of amyloidosis, it accelerates decline.
TRP cation channels combine with extrasynaptic NMDA glutamate receptors to set off mitochondrial meltdown and cell death. Blocking the interaction stops excitotoxicity.
Technical limitations may have misrepresented the transcriptional state of these cells, obscuring detection of their activation signature in frozen postmortem tissue from Alzheimer’s brain.
Two papers report that skin samples from people with Parkinson’s disease contain α-synuclein seeds that can be robustly amplified, paving the way for a reliable test for the disease.
Reducing levels of monounsaturated fatty acids lowered α-synuclein toxicity and prevented movement symptoms in mice. Scientists say the data boost the α-synuclein tetramer hypothesis.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
Most pathways that emerged were common between African Americans and non-Hispanic whites, though some individual variants differed. Kidney development jumped out as a possibly unique aspect of AD in African Americans.
Armed with snazzy new hardware, scientists solve protein structures to a resolution of 1.22Å. Cryo-EM now rivals X-ray crystallography.
A survey of 16 purported conformation-specific antibodies found that most bound nearly equally well to oligomers and fibrils, and weakly to monomers.
A new single-nucleus RNA-Seq study of 3,900 endothelial cells finds a boost in angiogenesis and antigen presentation genes, drawing attention to the vascular component of AD.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
Phospholipase C-γ2 acts downstream of TREM2 to rev up beneficial inflammation, phagocytosis, and cell survival.