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.
New data questions whether LRRK2’s kinase activity contributes to Parkinson’s, finding instead that absolute levels of the protein matter more.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
A Phase 2 trial suggests that the drug PBT2 is generally safe for Huntington’s patients. The drug's sponsor says it may have improved cognition, though experts remain unconvinced.
Neurons in mice spit out monomeric tau when electrically stimulated, hinting that neural activity may help drive the spread of pathological forms of tau in the brain.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
Researchers have sliced and digitally reassembled a famous brain in neuroscience to view its detailed three-dimensional architecture.
Live imaging of the mouse brain offers a rare view of α-synuclein dynamics at presynaptic terminals, and raises questions about which form of the protein triggers synaptic dysfunction.
A new study proposes that two genetic risk factors for frontotemporal dementia interact, disrupting brain connectivity decades before symptoms.
New research strengthens the idea that microglia do far more than scour the brain for emergencies.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
In neurodegenerative disease, tau is in the dendrites, and scientists are beginning to flesh out ways to block what it does there.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.