Courtesy of CryoEM: GABAA Receptor in Close-Up View
Get up close and personal with the GABAA receptor, a key mediator of inhibitory signaling in the brain and a drug target in a wide range of disorders, including Alzheimer’s.
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Get up close and personal with the GABAA receptor, a key mediator of inhibitory signaling in the brain and a drug target in a wide range of disorders, including Alzheimer’s.
Chronic inhibition of protein synthesis, and slowing the dispersal of stress granules, contribute to neurodegeneration in C9ORF72 ALS/FTD.
In healthy neurons, small vesicles at the presynapse and larger ones in neurites harbor Aβ42, according to super-resolution microscopy.
Males are inflammatory, females are neuroprotective: Profiling of microglia from adult mice suggests sex-specific phenotypes, likely set at birth.
Roche and Prothena publish Phase 1b results for their antibody PRX002/RG7935.
Big data analyses correlate viral load with clinical, molecular, and pathological features of AD. Time to consider the pathogen hypothesis anew?
A large epidemiological study better defines the risk from hypertension. This may sharpen recommendations for prevention.
Two papers report that the ApoE4 allele triggers both hallmarks of AD in iPSC-derived cultures, in contrast to its minimal effects in mouse neurons.
Overexpression of synaptojanin 1 leads to hippocampal place cell dysfunction in mice. Could it contribute to memory problems in AD?
In an unselected cohort, amyloid-PET scans changed clinical diagnoses and treatment plans for a quarter of participants.
Study suggests a diabetes drug under investigation for both Parkinson’s and Alzheimer’s diseases acts by quieting microglia and shutting down the pathological activation of astrocytes.
After veru- and atabecestat, now a third β-secretase inhibitor, by Eli Lilly and AstraZeneca, is being pulled from ongoing Phase 3 trials of symptomatic Alzheimer’s disease.
Though the dipeptides interacted with many proteins in cell culture, they associated specifically with ribosomes in the human brain.
In mice, antisense oligonucleotides that splice out more than half of the Aβ peptide drive down its levels in the brain.
By prying open chromatin, neurofibrillary tau may expose dormant transposable elements for transcription.
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