Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
The same endothelial cell response is found in various models of brain disease.
Prior research has focused on microglia interacting with synapses. New data show they also deal directly with the neuronal cell body. Like little conference rooms, specialized junctions host this communication.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
Cataloguing enhancer-promoter interactions in the four major cell types of the brain, researchers found that Alzheimer’s risk variants predominantly appeared in microglial enhancers.
Loss-of-function variants in the demethylase TET2 raise a person’s risk for early and late-onset Alzheimer’s, as well as FTD and ALS, suggesting a common mechanism.
In seven papers, researchers presented a dazzling set of findings gleaned from 125,748 exomes and 15,708 genomes housed in a new database. Tidbits emerge on tau, LRRK2, and other proteins implicated in neurodegeneration.
As mice age, a busy receptor-mediated protein transport across the barrier wanes; inhibiting an alkaline phosphatase restores it. Meanwhile, the aging barrier becomes generally leaky to large molecules.
Behold single proteins on the move: Super-resolution microscopy of living cells suggests the infamous protease does not form complexes with other secretases in the plasma membrane—in mouse fibroblasts, that is.
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.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.