New findings reinforce the idea that dementia with Lewy bodies can be pathologically classified as two different and distinct disease types.
Chronic gut inflammation can trigger the clumping of alpha-synuclein in the walls of the colon, a new study reports. Researchers found chronic inflammation in the gut during early life can exacerbate the clumping of alpha-synuclein in the brains of older mice. The findings add to a growing body of evidence which links gut health to Parkinson's disease.
A new model of Parkinson's disease sheds light on the asymmetrical motor symptoms, and other disorders, associated with this disease.
Study sheds new light on the damage alpha-synuclein does to neurons in Parkison's disease patients.
Researchers have discovered a series of misfolded alpha-synuclein protein structures never previously observed. The alpha-synuclein fibers were larger than previously reported and adopted a striking variety of shapes. The work lays the foundation for a detailed analysis of misfolded alpha-synuclein structures and could provide a better understanding of the neurobiology of Parkinson's disease.
Researchers have identified two different shapes of alpha-synuclein associated with multiple systems atrophy (MSA) and Lewy body dementia. The structure of the protein is helical in MSA, causing the symptoms to occur more quickly and aggressively. In Lewy body dementia, the protein takes on a cylindrical form.
T cells that react to alpha-synuclein are most abundant in the early stages of Parkinson's disease but tend to disappear as the disease progresses. Signs of autoimmunity can appear in Parkinson's patients up to ten years before a diagnosis of the neurodegenerative disease. The detection of T cell response could be an early biomarker for Parkinson's, long before the physical symptoms begin to manifest.
Natural killer cells may play a critical role in regulating and restraining neuroinflammation and protein clumping associated with Parkinson's disease.
Two regions outside of the non-amyloid-beta-component play a critical role in controlling amyloid formation of alpha-synuclein.
Using mouse models, researchers seeded alpha-synuclein aggregates in gut neurons and discovered the clumps can travel to neurons in the brain.
Ambroxol, a medication approved to treat coughs, may slow the progression of Parkinson's disease. The medication is able to effectively cross the blood-brain barrier and increases levels of GCase in patients' brains. Ambroxol also appears to reduce Parkinson's-related alpha-synuclein levels.
10% of patients diagnosed with Parkinson's disease are between the ages of 21 and 50. For those with young-onset Parkinson's disease, researchers report the foundations for the disease may have been apparent before they were born. The study also points to a drug, currently approved to treat precancerous skin growths, that has the potential to reduce elevated levels of alpha-synuclein.
