CURE ALZHEIMERS DISEASE :NEW GENETIC CULPRIT FOUND COULD HELP ALZHEIMERS Patients
3,587 views · Published 18 October 2017 · 12:26 · Indexed 21 September 2026
Channel: Healthy Lifestyle · 2017 · Education
Alzheimer's disease is a progressive neurodegenerative disorder, thought to be caused by buildup of proteins in the brain. But there is increasing evidence that different biological processes are at the heart of the disease, providing scientists with a different approach to possible therapies. In a plenary session delivered at the Alzheimer's Association International Conference (AAIC) 2017, held in London, United Kingdom, Julie Williams, Ph.D. - a professor in the Division of Psychological Medicine and Clinical Neurosciences at Cardiff University in the U.K. - challenged the traditional views of Alzheimer's disease by saying that "immunity is playing a significant role" in the disease. Alzheimer's disease is the sixth leading cause of death in the United States, affecting more than 5 million adults in the country. The traditional view is that proteins accumulate in the brains of patients, leading to neuronal death. The culprits are the amyloid beta peptide and the tau protein. Amyloid beta is produced when a short section of the amyloid precursor protein (APP) is severed. The function of the peptide in normal brain function is not known, but some evidence points toward a role in neurons. In Alzheimer's disease, amyloid beta accumulates in plaques in the spaces between neurons. Tau is a structural protein, important for neuronal function. But in Alzheimer's, tau does not function properly and accumulates in tangles in neurons. How this contributes to cell death is unknown, but there is new evidence that shows that abnormal tau processing can lead to toxic effects. How are scientists challenging the traditional view that abnormal protein buildup in the brain is to blame for the neurodegeneration seen in Alzheimer's disease? Joint efforts to identify new genetic variants Until 2009, only four genes were known to be associated with Alzheimer's disease. Mutations in three of these - APP, presenilin 1, and presenilin 2 - cause the inherited form of Alzheimer's. This typically develops early in life, between the ages of 30 and 50. It is also known as early-onset Alzheimer's disease. Less than 1 percent of Alzheimer's disease patients have this inherited form of the condition, in which an overproduction or abnormal folding of amyloid beta in the brain can be observed. The majority of patients have the sporadic form of Alzheimer's. Despite the fact that mutations in the apolipoprotein E gene (APOE) were known to be involved in susceptibility and earlier age of onset, only a subset of patients have the variant associated with the disease. Predicting an individual's risk of developing the disease with accuracy is, therefore, a challenge. For many years, there was a serious lack of progress in research looking to establish the underlying causes of susceptibility. Today, we know that sporadic Alzheimer's disease has a large genetic component, with its heritability being in the range of 58 to 79 percent. This means that other genetic variants must be involved. Advances in genetics and technology led to a breakthrough, in 2009, that saw Prof. Williams and other researchers identify three new genes associated with Alzheimer's disease using genome-wide association studies (GWAS). Prof. Williams told the audience at the AAIC that it very quickly became clear that future discoveries using this type of genetic analysis would be dependent on data from large numbers of patients being available. To her, the only way to achieve this would be to collaborate with other teams around the world. At the AAIC in 2010, held in Hawaii, the International Genomics of Alzheimer's Project (IGAP) was born. IGAP is a collaboration of four large research consortia, led by Prof. Williams and other scientists across the U.S. and Europe. IGAP researchers and other scientists have now identified 30 genes and genetic locations across the human genome that are involved a person's susceptibility to Alzheimer's. But what can scientists do with this new genetic information?
