Welcome to your daily round-up of everything happening in the world of neurorehabilitation.
AI speeds up drug design for Parkinson’s by ten-fold
Researchers have used artificial intelligence techniques to massively accelerate the search for Parkinson’s disease treatments. The researchers, from the University of Cambridge, designed and used an AI-based strategy to identify compounds that block the clumping, or aggregation, of alpha-synuclein, the protein that characterises Parkinson’s. The team used machine learning techniques to quickly screen a chemical library containing millions of entries, and identified five highly potent compounds for further investigation. Parkinson’s affects more than six million people worldwide, with that number projected to triple by 2040. No disease-modifying treatments for the condition are currently available. The process of screening large chemical libraries for drug candidates – which needs to happen well before potential treatments can be tested on patients – is enormously time-consuming and expensive, and often unsuccessful. Using machine learning, the researchers were able to speed up the initial screening process by ten-fold, and reduce the cost by a thousand-fold, which could mean that potential treatments for Parkinson’s reach patients much faster. The results are reported in the journal Nature Chemical Biology.
Alzheimer’s disease progresses faster in people with Down syndrome
Nearly all adults with Down syndrome will develop evidence of Alzheimer’s disease by late middle age. A new study by researchers at Washington University School of Medicine in St. Louis shows that the disease both starts earlier and moves faster in people with Down syndrome, a finding that may have important implications for the treatment and care of this vulnerable group of patients. The findings were part of a study, available online in Lancet Neurology, comparing how Alzheimer’s develops and progresses in two genetic forms of the disease: a familial form known as autosomal-dominant Alzheimer’s disease, and Down syndrome-linked Alzheimer’s.
“Currently, no Alzheimer’s therapies are available for people with Down syndrome,” said co-senior author Beau Ances, MD, PhD, the Daniel J. Brennan Professor of Neurology. Ances, who cares for patients with Down syndrome, explained that people with the developmental disability historically have been excluded from Alzheimer’s clinical trials. “This is a tragedy because people with Down syndrome need these therapies as much as anyone,” Ances continued. Down syndrome is caused by the presence of an extra chromosome 21. That extra chromosome carries a copy of the APP (amyloid precursor protein) gene, meaning that people with Down syndrome produce far more amyloid deposits in their brains than is typical. Amyloid accumulation is the first step in Alzheimer’s disease. For people with Down syndrome, cognitive decline often occurs by the time they reach their 50s.
New findings on cellular lineage
A group of researchers at University of California San Diego School of Medicine led an investigation that offers new insight into the development of the human forebrain. The study provides a greater understanding of how the human brain develops at the cellular level. It also presents evidence for the existence of the source of inhibitory neurons (dInNs) in the human brain that differ from origins in other species like mice, a common lab animal used in brain studies. The group outlined their findings in a paper recently published in the journal Nature. The forebrain, or cerebral cortex, is the largest part of the brain, important for a wide range of function, ranging from cognitive thought, vision, attention and memory. Neurons are cells that serve as the individual circuits of the brain. Inhibitory neurons usually function as a kind of neural “off” switch, as opposed to the “on” switch of excitatory neurons.
“Humans have a very large and wrinkled cortex that likely supports higher cognitive functions compared with other species, such as rodents,” Gleeson explained. He said that the inhibitory neurons in mice have an origin from deep within the developing brain. The current study puts that model to test by assessing cellular lineage. They found existence of dInNs, which are absent in mice. He said finding evidence for this specific type of neuron in humans opens the door to greater understanding how the human brain is special.
Lewy bodies research progresses
A new study from Van Andel Institute scientists offers a first look into the complex molecular changes that occur in brain cells with Lewy bodies, which are key pathological hallmarks of Parkinson’s disease and some dementias. The findings reveal that brain cells with Lewy bodies exhibit a specific gene expression pattern akin to a disease-related fingerprint. “We’ve long known that Lewy bodies play a role in Parkinson’s and other neurodegenerative diseases but there are still many unanswered questions. Why are some cells more susceptible to Lewy bodies than others? How do Lewy bodies actually affect cells?” said VAI Assistant Professor Michael Henderson, Ph.D., the study’s corresponding author. “Our findings are an important starting point for better understanding how cells respond to Lewy bodies, which is an area of great potential for informing new therapies.” See more on the study here.
