A high dose of nicotinamide, tested as a treatment for early-stage Alzheimer’s, showed no significant impact on reducing harmful tau proteins in the brain.
A rare genetic variant, APOE3 Christchurch, delays Alzheimer's onset by years in high-risk individuals, offering insights into disease resilience. This discovery could guide new treatments targeting similar protective pathways for Alzheimer’s prevention and therapy.
New research suggests Alzheimer's drugs may improve cognition by increasing Aβ42 levels rather than just reducing plaques, challenging the amyloid cascade hypothesis and pointing to new therapeutic strategies focused on restoring soluble Aβ42 to maintain brain health.
The MIND diet slows cognitive decline in older adults, with Black participants requiring stricter adherence for benefits. Racial and gender differences suggest broader social, lifestyle, and biological factors influence the diet's effectiveness.
Researchers observed that amyloid-beta and tau proteins are associated with a transition from hyperactivity to slower brain activity, which aligns with declines in attention and memory, suggesting potential early indicators of Alzheimer’s disease progression.
APOE4 carriers had higher blood-brain barrier permeability, even without cognitive decline or amyloid beta buildup, suggesting early vascular changes that may be linked to Alzheimer’s risk and neurodegeneration.
A study found untreated hypertension increases Alzheimer's risk by 36% and non-Alzheimer's dementia risk by 69%. Treating hypertension lowers these risks, highlighting the importance of antihypertensive medication.
Researchers discovered that Alzheimer’s disease progresses in two phases: a slow, early phase with silent damage to specific brain cells, followed by a faster, symptomatic phase. These insights could lead to earlier detection and targeted treatments.
Researchers have discovered that non-neuronal brain cells, oligodendrocytes, produce about 30% of amyloid plaques in Alzheimer’s disease. This challenges the neuron-focused understanding of plaque formation and could lead to new therapeutic strategies targeting oligodendrocytes to slow disease progression.
Lower caffeine consumption was linked to a higher risk of memory impairment and worse Alzheimer's disease biomarkers, suggesting caffeine might offer protective effects against cognitive decline. However, more research is needed to confirm any direct benefits.
New research suggests that exposure to artificial light at night may increase the risk of Alzheimer’s disease, particularly in younger people, highlighting light pollution as a potential factor in the rise of neurodegenerative conditions.
Researchers discovered that some brain cells age faster than others, especially in people with Alzheimer’s disease. Women’s brains also show more of these rapidly aging cells, which may increase their risk for neurodegenerative disorders.
UCLA researchers have discovered a compound, DDL-920, that restores memory and cognitive function in Alzheimer’s model mice by enhancing brain gamma oscillations, offering a potential new treatment that goes beyond slowing disease progression.
Alzheimer’s disease risk is more strongly influenced by maternal genetics, with higher amyloid plaque levels in those with a maternal history of memory loss, suggesting mitochondrial dysfunction may play a key role.
Scientists have uncovered a significant clue to understanding why some individuals are more susceptible to Alzheimer’s disease.