Researchers from Boston University School of Medicine (BUSM) have found that higher leptin (a protein that controls weight and appetite) levels were associated with a lower incidence of Alzheimer's Disease (AD) and dementia. The study, which appears in the December 16th issue of the Journal of the American Medical Association, may open pathways for possible preventive and therapeutic interventions.
Imaging tests may be able to detect the early signs of Alzheimer's disease long before it begins to affect memory, a finding that may lead to earlier, more effective treatments, US researchers said on Monday.
They said healthy people who have an abnormal buildup of a protein in the brain linked with Alzheimer's disease have a higher risk of developing the disease.
When it comes to understanding a disease as complex as Alzheimer's, the more the better - genes, that is. In September, 15 years since the last discovery of its kind, scientists finally identified a new set of genes that may contribute to the memory-robbing disorder. Two groups of researchers, working separately, homed in on three genes linked to the late-onset form of the disease, the type that hits people in their 60s or later and accounts for 90% of Alzheimer's cases in the US.
Aging is the single greatest risk factor for Alzheimer's disease. In their latest study, researchers at the Salk Institute for Biological Studies found that simply slowing the aging process in mice prone to develop Alzheimer's disease prevented their brains from turning into a neuronal wasteland.
Stimulating the growth of new neurons to replace those lost in Alzheimer's Disease (AD) is an intriguing therapeutic possibility. But will the factors that cause AD allow the new neurons to thrive and function normally? Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that two main causes of AD amyloid-beta (aβ) peptides and apolipoprotein E4 (apoE4) impair the growth of new neurons born in adult brains.
A major discovery is challenging accepted thinking about amyloids -- the fibrous protein deposits associated with diseases such as Alzheimer's and Parkinson's -- and may open up a potential new area for therapeutics.
It was believed that amyloid fibrils -- rope-like structures made up of proteins sometimes known as fibres -- are inert, but there may be toxic phases during their formation which can damage cells and cause disease.
More than half of HIV patients experience memory problems and other cognitive impairments as they age, and doctors know little about the underlying causes. New research from Washington University School of Medicine in St. Louis suggests HIV-related cognitive deficits share a common link with Alzheimer's-related dementia: Low levels of the protein amyloid beta in the spinal fluid.
The research group of Professor Magdalena Gotz of Helmholtz Zentrum Munchen and Ludwig-Maximilians-Universitat (LMU) Munich has made a significant advance in understanding regenerating processes in the brain. The researchers discovered progenitor cells which can form new glutamatergic neurons following injury to the cerebral cortex. Particularly in Alzheimer's disease, nerve cell degeneration plays a crucial role. In the future, new therapeutic options may possibly be derived from steering the generation and/or migration mechanism.
Universitat Autonoma de Barcelona (UAB) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps to boost the production of the brain's stem cells - neurogenesis - and strengthens their differentiation in different types of neuron cells.
Alzheimer's disease is thought to be caused by the build-up of a brain peptide called amyloid-beta. That's why eliminating the protein has been the focus of almost all drug research pursuing a cure for the devastating neurodegenerative condition.
But that may be counterproductive, says Dr. Inna Slutsky of Tel Aviv University's Department of Physiology and Pharmacology, Sackler Faculty of Medicine. Her recent research demonstrates that amyloid-beta is also necessary to maintain proper brain function.
These findings may shake the foundations of Alzheimer's research.