By identifying potential genetic causes of Lewy body dementia (LBD), researchers hope to gain a better understanding of the devastating neurodegenerative disorder, for which there are no treatments. It is already known that LBD, Parkinson’s disease (PD), and Alzheimer’s disease (AD) are all caused by clumps of proteins that build up in the nerve cells of the brain (alpha-synuclein in LBD and PD, tau in AD). The three diseases have some overlapping symptoms and related features of neurodegeneration.
Although some symptoms of Parkinson’s disease (PD) can be controlled by medication, the hope of researchers, patients, and clinicians is that we can discover a treatment that can stop or reverse the course of PD and eventually find a cure. Central to developing disease-modifying treatments is an understanding of the role of alpha-synuclein, a key protein found in everyone’s brain, that’s recognized as a cause of PD.
Alterity Therapeutics announced that it has received a second grant from The Michael J. Fox Foundation for Parkinson’s Research to continue its study of ATH434, a small molecule that targets alpha-synuclein, in Parkinson’s disease (PD).
Parkinson’s is a complicated neurological disorder that researchers are continuously working to understand. However, a lack of dopamine—a neurotransmitter responsible for our ability to control the way our bodies move (among many other things)—is widely recognized as a cause.
Recently, a team of researchers based in Israel evaluated whether certain proteins, known as bone morphogenetic proteins 5 and 7 (BMP5/7), could protect dopamine-producing neurons in the brains of mice from damage caused by the misfolded alpha-synuclein protein, another major player in the cause of Parkinson’s disease.
The researchers found that not only did BMP5/7 reverse the alpha-synuclein-induced loss of dopamine-producing neurons, but it also reduced the accumulation of alpha-synuclein in the brain and prevented motor impairment in the study mice. The authors conclude that BMPs are a promising option in the development of disease-modifying treatments for Parkinson’s, an area of significant unmet need.
MODAG, a German biotechnology company, announced that it would begin an in-patient clinical trial of anle138b, a disease-modifying treatment for synucleinopathies such as multiple system atrophy (MSA) and Parkinson’s disease (PD).
The two companies announced an exclusive collaboration agreement that aims to develop treatments that target alpha-synuclein, a protein whose accumulation in the brain causes several neurodegenerative disorders, such as Parkinson’s disease and dementia with Lewy bodies.
A group of international experts responded to the publication of the recent Systemic Synuclein Sampling Study (S4), which found alpha-synuclein to be a specific—but not sensitive—marker of Parkinson’s disease. Their letter details how the study’s methods, rather than the specificity of alpha-synuclein as a marker for Parkinson’s disease, may have produced the results.