Despite decades of starts and stops, new treatments and key genetic discoveries are giving researchers great hope for slowing or eventually preventing Alzheimer’s disease.
In clinical trials, lecanemab slowed disease progression by 27% and reduced the amount of plaque found in the brains of those with Alzheimer’s disease.
An 18-month treatment with lecanemab slows functional and cognitive loss by 27 per cent in people with mild Alzheimer’s disease. But this is only the first step towards a real cure.
Impaired insulin receptors in the blood vessels between the blood and the brain may contribute to the insulin resistance observed in Alzheimer’s disease.
Microglia, immune cells disguised as brain cells, are known as the janitors of the brain. Dialing up their usual duties just enough could provide an avenue to treat neurodegenerative disease.
Alzheimer’s may not be primarily a disease of the brain. It may be a disorder of the immune system within the brain. Beta-amyloid may not be an abnormal protein, but part of the brain’s immune system.
If replicated in humans, these findings could mean that targeting or boosting the circadian rhythm in Alzheimer’s patients, could help with managing the disease
The FDA approved Alzheimer’s disease drug aducanumab despite minimal evidence of its efficacy. Whether this decision ultimately hurts or helps patients depends on data researchers don’t yet have.
It was first officially described 115 years ago, but we still do not have a cure for Alzheimer’s disease. The human brain is extremely complex, and Alzheimer’s is its most complex disease.
Director, Evelyn F. and William L. McKnight Brain Institute Director, 1Florida Alzheimer’s Disease Research Center, Professor, Department of Neuroscience, College of Medicine University of Florida, University of Florida