A recent study revealed that amyloid-beta protein has been found in the brains of people as young as 20 years old. This protein is the plaque that forms on the brain in Alzheimer’s patients. Originally, the protein had only been found in the brains of much older patients. Its presence in such a young group of people shocked researchers.
Research co-author Changiz Geula and associates studied the brain tissue of 48 deceased individuals aged from 20 to 99. Thirteen people with no mental health issues, 14 people with dementia and 21 people with Alzheimer’s. They found amyloid-beta, an abnormal protein known to accumulate around neurons in the brains of senior citizens with Alzheimer’s. What surprised researchers was its presence in the brains of those much younger. This plaque can lead to Alzheimer’s disease and may explain the onslaught of early onset Alzheimer’s cases that are cropping up. Armed with this information, researchers and doctors can do what they must to treat and prevent this dangerous build-up, and Alzheimer’s, as early as possible.
Researchers paid particular attention to the basal forebrain cholinergic neuron. This neuron is especially susceptible to the ravages of Alzheimer’s disease. It is responsible for the brain’s ability to both pay attention and remember details. Researchers found amyloid-beta build-up around these delicate neurons. It is clear that clumps of the protein damage and even kill these neurons. What is particularly perplexing is how much of this dangerous protein remains in the general population, and not just senior citizens.
This was a very small study involving a centralized group of less than 50 people. Dr. Yvette Sheline, a neurology professor at the University of Pennsylvania issued a caveat. Although not directly involved in the Alzheimer’s study, she cautions against putting much weight into the study’s Alzheimer’s findings. She says that this study involved a small sample of brain tissue and concentrated solely on one specific neuron type. Although she concurs that it is “interesting” that amyloid concentration in the basal forebrain occurs so early, too many other variables are unaccounted for, including follow-ups and later mental health assessments. This would be impossible because only brain tissue and not live people were studied. There is no way to know whether Alzheimer’s would ever develop.
This begs the question of how to remove plaque from the brain before it causes damage. Researchers at the Mayo Clinic in Jacksonville, Florida have found that a protein called interlukein-6 (IL-6) removes plaque from the brain. This was done with rats who had Alzheimer’s disease, and not humans. It is not currently prescribed to treat Alzheimer’s but there are other drug therapies to combat Alzheimer’s, five in all. Remilyn, Exelon, Aricept and Cognex are cholinesterase inhibitors. These Alzheimer’s drugs prevent the breakdown of acetylcholine, an essential chemical for communication within the brain. The fifth drug, Nameda, is a mematine, a drug that helps with the confusion and reasoning problems associated with Alzheimer’s. T-187-MA is an Alzheimer’s drug that is in the clinical trial stage, with hopes to be on the market soon. It works like Namenda in that it protects the brain from too much glutamate, which also damages neurons. It has the added benefit of protecting the brain from Alzheimer’s.
Although much of the research involving Alzheimer’s drug therapy has focused on the amyloid-beta protein in the brain, recent findings are zeroing on the discovery of the protein oligomers in the Alzheimer’s-affected brain. A recent UCLA study showed that recent Alzheimer’s drug clinical trials are failing because they focus on the amyloid-beta protein and not oligomers. Researchers think the focus should be on oligomers, which appear in the brain years before the plaque from amyloid-beta appears.
By Danielle Branch