AD but no Amyloidβ? Researchers at AAIC 2013 theorized on the pathology underlying this form of dementia.
Protein strains may underlie different tauopathies, according to researchers presented at this year's AAIC meeting in Boston.
A study suggests that genes involved in Aβ production and endocytosis mediate ApoE4’s role in Alzheimer’s disease.
While mice sleep, neurons sprout synapses to solidify fresh skills, according to a new study. The brain also keeps amyloid-β levels low while we snooze.
Hunting for rare mutations that cause dementia, researchers have spotted, but not yet snagged, some tantalizing candidates.
A parkinsonism-associated ubiquitin ligase interacts with parkin to promote mitophagy.
Rare variants of AD share some common areas of brain atrophy, but are also unique by way of degeneration in specific functional networks that correspond with clinical symptoms.
Brain connections weaken years before cognition in sporadic and familial Alzheimer’s.
Preliminary data from Parkinson’s Progression Markers Initiative suggests that cerebrospinal fluid biomarkers distinguish the most rapidly progressing form of Parkinson’s.
Before cognition falters, Alzheimer’s disease wreaks havoc on synapses, the brain’s subcellular communication hubs.
Brain imaging distinguishes ALS patients with C9ORF72 expansions from those with other forms of the disease.
The experimental drug NitroMemantine protects synapses from Aβ oligomer toxicity in mice by blocking extrasynaptic NMDA receptors.
Eating fewer saturated fats and simple sugars reduces harmful forms of Aβ in the cerebrospinal fluid, scientists report.
In a series of eight reviews, titled "Focus on Neurotechniques," researchers describe how approaches such as optogenetics and stem cells are revolutionizing neuroscience.
Using hormone therapy early in menopause neither helps nor harms cognition, researchers report.