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Studies Investigate Links Between Parkinsonís Disease and Alzheimerís Disease
- Oct 29 2013
Parkinson’s disease (PD) and Alzheimer’s disease (AD) are common neurodegenerative diseases associated with aging. People can develop both PD and AD, leading researchers to consider whether there are links between the two diseases. Two new studies have found that the two diseases do not appear to share genetic characteristics but may be linked by proteins.
In the genetics study, published in the August 5 online edition of JAMA Neurology, researchers analyzed genome-wide association (GWA) studies of PD and AD to look for genetic variants shared by both diseases. The study was led by author Valentina Moskvina, Ph.D., of the Cardiff University School of Medicine in Wales, in collaboration with an international team that included researchers from the National Institutes of Health. The team reviewed GWA studies of thousands of people with AD and PD, to see if any genetic variants increased the risk of both diseases.
The second study, published in the July 3 online edition of Cell by a team from the University of Pennsylvania led by Virginia Lee, Ph.D., investigated proteins found in AD and PD. Most neurodegenerative diseases are characterized by the accumulation of abnormal forms of certain proteins – for example, tau and amyloid in AD and alpha-synuclein in PD. Studies have shown some overlap in the pathology of AD and PD: more than 50 percent of people with AD show alpha-synuclein deposits and people with PD commonly have tau deposits. To better understand any relationship, researchers conducted experiments with alpha-synuclein involving mice and cell cultures.
- In reviewing genetics or GWA studies, researchers found no common genetic variants that increase the risk of developing both diseases.
- In experiments with alpha-synuclein, the protein which is primarily associated with Parkinson’s disease pathology, researchers found that specific strains of the protein help the accumulation in brain cells of the tau protein. Tau is primarily associated with Alzheimer’s disease, but is also found in PD.
What Does It Mean?
This study looked at the relationship between Parkinson's and Alzheimer's. Questions about a possible link have been raised by scientists to better understand whether people with Parkinson's who experience dementia at at risk for Alzheimer's or whether dementia is instead a part of Parkinson' disease. Results indicate that PD and AD are not linked by genes but do appear to be linked by proteins.
Supporting the hypothesis that PD and AD are not related is the genetics study, which failed to find any common variants that increase risk of both diseases. Based on this evidence, people who are genetically predisposed to developing PD do not automatically have an increased genetic risk for the other. This is the first study to examine this question.
Meanwhile, the second study indicates that PD and AD are related, as it relates to protein accumulation in the brain. While both diseases are primarily caused by deposits of unique proteins in the brain, they also have protein deposits in common. The Cell study found that there are certain strains of the alpha-synuclein protein associated with PD that can encourage the accumulation of the tau protein associated with Alzheimer’s.
This discovery sheds light on how proteins create disease and may explain how people with PD develop AD like changes in the brain. Further research may eventually lead to new treatments that target the disease-causing proteins and prevent their accumulation.
Reference: Moskvina V, Harold, D, Russo G, et al. (2013) Analysis of Genome-Wide Association Studies of Alzheimer Disease and of Parkinson Disease to Determine If These 2 Diseases Share a Common Genetic Risk. JAMA Neurol DOI: 10.1001/jamaneurol.2013.448 http://dx.doi.org/10.1001/jamaneurol.2013.448
Reference: Lee, V MY, Guo JL, Daniels JP, et al. (2013) Distinct Alpha-Synuclein Strains Differentially Promote Tau Inclusions in Neurons. Cell 154, 103-117. DOI:10.1016/j.cell.2013.05.057 http://dx.doi.org/10.1016/j.cell.2013.05.057
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Source Date: Sep 19 2013