Researchers detail the complex interaction between alpha synuclein and the prion protein PrPc.
Researchers have created an artificial enzyme that stops alpha-synuclein from spreading. The findings could have positive implications for the treatment of Parkinson's disease.
People with two common types of dementia, Lewy body dementia, and Alzheimer's disease, have unique walking patterns. The gait type signals subtle differences between the two disorders. Those with Lew body dementia change their steps more, varying the step time and length. They also display more asymmetry in movement compared to those with Alzheimer's disease. Researchers say gait could be a clinical biomarker for dementia subtypes.
A new model of Parkinson's disease demonstrates how abnormal alpha-synuclein proteins gradually spread from brain areas implicated in early stages of the disease to other regions of the brain.
Using a tiny dose of the leukemia drug nilotinib, researchers halt the accumulation of toxic proteins linked to Parkinson's diseases in the brains of mice.
Study identified five genes, including two novel genes, associated with Lewy Body dementia. Researchers also found the genetic profiles of patients with LBD showed higher chances of also suffering from Alzheimer's and Parkinson's disease than other age-matched control subjects.
Researchers report those who have had appendectomies have a reduced risk of developing Parkinson's disease. A new study reveals the appendix acts as a reservoir for proteins associated with the neurodegenerative disease.
A new study reports on how the clinical profiles of Lewy body dementia differ from Alzhiemer's or Parkinson's disease.
Lewy body disorders, including Parkinson's disease and Lewy body dementia, comprise of two distinct subtypes. One subtype originates in the peripheral nervous system (PNS) of the gut and spreads to the brain. The other originates in the brain, or enters the brain via the olfactory system, before spreading to the brainstem and PNS.
Researchers investigate the role the BMI1 gene plays in the onset and development of Alzheimer's disease. The study reports the loss of BMI1 triggers and increased production of amyloid beta and decreases neural ability to eliminate the protein.