A protein called Aβ is thought to cause neuronal death in Alzheimer’s disease (AD). Aβ forms insoluble aggregates in the brains of patients with AD, which are a hallmark of the disease. Aβ and its propensity for aggregation are widely viewed as intrinsically abnormal. However, in new work, Kumar et al. show that Aβ is…
DetailsSponsored by the UC Office of the President with a foundational grant of $4 million, the UC Cures initiative invited hundreds of laboratories throughout the 10-campus system to find new answers to Alzheimer’s disease and related disorders.
Nancy Reagan, the influential and stylish wife of the 40th president of the United States who unabashedly put Ronald Reagan at the center of her life but became a political figure in her own right, died on Sunday at her home in Los Angeles. She was 94.
Howard Feldman of University of British Columbia is known for seminal research in dementias; UC launches new $4 million Alzheimer’s disease initiative.
The model developed by the three researchers Prof Markus Werning, Prof Sen Cheng and Prof Thomas Suddendorf differs from other approaches with regard to one major aspect: it suggests a new relationship between mental time travel and episodic memory.
Levels of neurogranin, a cerebrospinal fluid (CSF) biomarker for synaptic loss, were elevated in patients with Alzheimer’s disease (AD) compared with cognitively normal individuals. Neurogranin levels also predicted progression from mild cognitive impairment (MCI) to AD dementia, researchers reported here on Monday at the Alzheimer’s Association International Conference (AAIC).
Examining post-mortem tissue from the brains of people with Alzheimer’s disease, Stanford University School of Medicine investigators identified what appear to be iron-containing microglia in a particular part of the hippocampus, a key brain structure whose integrity is critical to memory formation.
Two UC San Diego Researchers to Lead Alzheimer’s Disease Cooperative Study.
This finding provides the most compelling evidence to date of brain inflammation, and more specifically microglial activation, in MDE. The correlation between higher ACC TSPO VT and the severity of MDE is consistent with the concept that neuroinflammation in specific regions may contribute to sickness behaviors that overlap with the symptoms of MDE.
Remarkably, this boost in cognition occurred despite the accumulation of Alzheimer-related toxins in the brain, such as amyloid-beta and tau.