A massive study of medical and genetic data shows that people with a particular version of a gene involved in immune response had a lower risk of Alzheimer’s and Parkinson’s disease. 175 researchers from 150 institutions in roughly 25 countries contributed to the study.
The facts are shocking. It has been estimated that 20% of men and women carry a version of a specific gene . The gene appears to be largely unsung and unstudied. However, new research shows that it has been shown to offer protection against both Parkinson’s Disease as well as Alzheimer’s. The study was released by disease, Stanford Medicine investigators and their colleagues.
These 20% are some lucky people. Further testing can make it so they can benefit from the gene sequence. Furthermore, this gene could aid vaccine that might be able to slow or stall the progression.
The study included genetic data from 100’s of thousands of individuals. The people in the study were of a diverse ancestries.
In addition, the population was spread over several continents. The results were encouraging. It showed that carrying this gene version reduced people’s chances of contracting either Parkinson’s or Alzheimer’s by over 11 percent.
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The study was focuses on a protein named TAU.
The evidence showed a correlation in the way of aggregating in the brains of Alzheimer’s patients. The same may be said in the development of Parkinson’s disease. It is still a mystery how this occurs in the brain.
The study was authored by:
- Emmanuel Mignot, MD, PhD, the Craig Reynolds Professor in Sleep Medicine and aprofessor of psychiatry and behavioral sciences
- Michael Greicius, MD,
- Asad Jamal Professor and a professor of neurology and neurological sciences
- Jean-Charles Lambert, PhD, director of research for Inserm at the University of Lille in France
- Yann Le Guen, PhD, assistant director of computational biology in Stanford Medicine’s quantitative sciences unit
- Guo Luo, PhD, an instructor of sleep medicine
- Former postdoctoral scholar Aditya Ambati, PhD
- Vincent Damotte, PhD, a bioinformatician associated with Lambert’s group.
The protective allele identified in the study is called DR4
The Stanford Medicine team sourced 35-40 medical and genetic databases from numerous countries . The countries included, Europe, East Asia, the Middle East, and the Americas.
“In an earlier study we’d found that carrying the DR4 allele seemed to protect against Parkinson’s disease,” Mignot said. “Now, we’ve found a similar impact of DR4 on Alzheimer’s disease.”
The data included over 40,000 Parkinson sufferers and well over 110,000 people with Alzheimer’s disease. The scientists made the comparisons. The showed that the incidence and age of onset of Alzheimer’s and Parkinson’s among people with DR4 makes a big difference, The data supports that those without it had a roughly 11 percent lower risk than people with DR4.
“That this protective factor for Parkinson’s wound up having the same protective effect with respect to Alzheimer’s floored me,” Mignot said. “The night after we found that out, I couldn’t sleep.”
Having the DR4 gene has correlated with a future onset of Parkinson’s . This applies even though neurofibrillary tangles aren’t y seen in the disease.
This study hints that tau is an important factor in Alzheimer’s,. In fact, it may turn out to also play some kind of role in Parkinson’s.
A cell’s outer membrane keeps the cell’s insides in and its outsides out
But the cell membrane does more. It also serves as a display window. This window can show the outside what is inside. This will expose fragments of the proteins inside it to the immune system. When the immune system spots a surface peptide it’s never seen before it springs into action. It may start a powerful attack on cells that are displaying that peptide. Now and then, the attack is a case of mistaken identity For example, autoimmunity is such a phenomenon. In addition, researchers tested all the biologically likely chemical modifications each of the peptides can accrue inside a cell. Mignot thinks DR4 is involved in what has been called “protective autoimmunity”.
