Study: Misfolded alpha-synuclein protein key to early detection of Parkinson’s disease

The presence of a misfolded alpha-synuclein protein can be used to determine if people have Parkinson’s disease, according to a new study using technology developed by a researcher at UTHealth Houston. This biomarker could pave the way for the development of better diagnostic tools and new treatment options for the disease.

Johns Hopkins Medicine Scientists Create Nanobody That Can Punch Through Tough Brain Cells and Potentially Treat Parkinson’s Disease

Johns Hopkins Medicine researchers have helped develop a nanobody capable of getting through the tough exterior of brain cells and untangling misshapen proteins that lead to Parkinson’s disease, Lewy body dementia, and other neurocognitive disorders caused by the damaging protein.

Gut-Brain Connection Research Gets Boost of $8.9 Million

Johns Hopkins Medicine is one of three research institutions with scientists awarded $8.9 million to study the growing body of evidence that Parkinson’s disease originates among cells in the gut and travels up the body’s neurons to the brain. The research aims to develop treatments to prevent or halt progression of the disease.

Hopkins Med News Update

NEWS STORIES IN THIS ISSUE:

-Study: Race and Ethnicity May Impact Prevalence and Treatment of Heart Valve Dysfunction
-Johns Hopkins Medicine Suggests Eliminating Nerve Cell Protein May Stop ALS, Dementia
-Researchers Tell Doctors to Avoid Routine Urinary Tests for Older Patients with Delirium
-Johns Hopkins Medicine Researchers Show How Air Pollution May Cause Chronic Sinusitis
-Researchers ID Location on Brain Protein Linked to Parkinson’s Disease Development
-COVID-19 News: The Return of Onsite Schooling — and How to Keep Your Kids Safe from COVID

Will reduction in tau protein protect against Parkinson’s and Lewy body dementias?

A study suggests that reducing tau protein in brain neurons will not protect against Parkinson’s disease and Lewy body dementias. If borne out, this result differs from Alzheimer’s disease, where reducing endogenous tau levels in brain neurons is protective for multiple models of the disease.