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.
Much like people with Alzheimer's, mice modelling the disease experience seizures. New research suggests that APP, and not Aβ, makes their neurons hyperexcitable.
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.
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.
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.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
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.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
Vitamin E slows functional deterioration in people with mild to moderate Alzheimer's disease, according to a new study.
Evidence builds that amyotrophic lateral sclerosis and frontotemporal lobar degeneration sit on the same pathological spectrum, but scientists are unsure how the disease marker TDP-43 fits in.
Using the transferrin receptor to deliver therapeutics to the brain is tricky—antibodies that bind too tightly stall in blood vessel cells and shut down transport.
Proteins that interact with the Parkinson’s risk gene LRRK2 point to protein trafficking and degradation as causes of pathogenesis.