A study finds that disruptions in the body's internal clock, especially weaker circadian rhythms and later activity peaks, are linked to a higher risk of developing dementia in older adults, suggesting potential benefits of circadian rhythm interventions for prevention.
A promising experimental drug called NU-9 has shown potential in preventing Alzheimer's disease in mice by targeting toxic amyloid-β protein subtypes early in the disease process, with future human trials and early diagnostic tests on the horizon.
A study suggests that oral bacteria like Streptococcus mutans can migrate to the gut, produce metabolites such as ImP, and potentially contribute to Parkinson’s disease by affecting neurons and promoting neuroinflammation, highlighting new therapeutic targets involving the microbiome.
An experimental drug called NU-9 developed at Northwestern University shows promise in preventing Alzheimer's disease by targeting toxic amyloid beta oligomers early in the disease process, potentially delaying or stopping memory loss and neurodegeneration.
Researchers have uncovered how a rare genetic mutation in the GPX4 gene causes neurodegeneration through ferroptosis, a form of cell death linked to oxidative damage, providing new insights into diseases like Alzheimer's and childhood dementia.
A study in mice shows that blood from young animals has protective effects against Alzheimer's disease by reducing amyloid plaque buildup and cognitive decline, while aged blood accelerates disease progression, highlighting the potential of targeting blood-borne factors for therapy.
Scientists at Johns Hopkins have found that hydrogen sulfide, a gas produced in the body and present in flatulence, could protect against Alzheimer's disease by improving cognitive and motor functions, with potential for new drug development.
Scientists at Johns Hopkins suggest that small doses of hydrogen sulfide, a gas produced naturally in the body and associated with foul smell, may help protect against Alzheimer's disease by improving brain cell signaling and reducing protein clumping, as demonstrated in mouse studies.
Researchers at Penn State discovered that stress-sensitive type-one nNOS neurons regulate brain blood flow and neural activity; their loss due to chronic stress may contribute to brain health decline and neurodegenerative diseases like dementia, highlighting a new environmental risk factor.
Research from Osaka Metropolitan University shows that while the Alzheimer's drug lecanemab reduces amyloid plaques, it does not improve the brain's waste clearance system in the short term, highlighting the disease's complexity and the need for multi-targeted therapies.
A study published in Science Advances reveals that boosting NAD⁺ levels can restore memory and improve brain function in Alzheimer's disease models by correcting RNA splicing errors through the regulation of EVA1C, offering potential new therapeutic avenues.
Originally Published 2 months ago — by MindBodyGreen
A recent study published in Neurology shows that regular physical activity can slow brain aging and neurodegeneration, particularly in regions like the cortex and hippocampus, which are vital for memory and cognition. Engaging in consistent, moderate exercise such as walking, cycling, or dancing can help preserve brain structure and function, potentially delaying conditions like Parkinson's and Alzheimer's, and maintaining mental sharpness as we age.
Scientists at Weill Cornell Medicine discovered that free radicals produced in astrocytes' mitochondria contribute to dementia, and blocking these radicals with targeted compounds reduced inflammation and protected neurons in animal models, opening new avenues for treatment.
The article discusses how mitochondrial complex III-derived reactive oxygen species (ROS) in astrocytes amplify immune and metabolic changes that contribute to dementia pathology, highlighting the role of specific signaling pathways and potential therapeutic targets.
Disrupting the body's internal clock by inhibiting the circadian protein REV-ERBα in mice increases NAD+ levels, reduces tau pathology, and may offer a new approach to slowing or preventing Alzheimer's disease progression.