The most common gene mutation associated with Parkinson's alters cells circulating outside the brain, not within, offering a new understanding of what causes the disease.
Working with lab-grown human brain cells, Johns Hopkins researchers report they have uncovered a much sought-after connection between one of the most common genetic mutations in Parkinson's disease and the formation of fatty plaques in the brain thought to contribute to the destruction of motor neurons that characterize the disease.
Scientists at the Allen Institute and the University of Washington have developed a new low-cost technique for profiling gene expression in hundreds of thousands of cells.
To understand the link between aging and neurodegenerative disorders such as Alzheimer's disease, NIH scientists compared the genetic clocks that tick during the lives of normal and mutant flies. They found that altering the activity of a gene called Cdk5 appeared to make the clocks run faster than normal, and the flies older than their chronological age. This caused the flies to have problems walking or flying later in life, to show signs of neurodegeneration, and to die earlier.
The findings open the door to developing new treatments for a wide range of illnesses, from heart disease, diabetes and cancer to neurodegenerative disorders, including Parkinson's disease.
A new Tel Aviv University study suggests a novel way of treating the areas of the brain that apparently cause freezing of gait in patients with Parkinson's disease.
Researchers investigate the connection between misfolded proteins and the destruction of mitochondria in neurons.
A group of genes and genetic switches involved in age-related brain deterioration have been identified by scientists. The research found that changes to one of these genes, Dbx2, could prematurely age brain stem cells, causing them to grow more slowly. By comparing the genetic activity in brain cells from old and young mice, the scientists identified over 250 genes that changed their level of activity with age.
If the sense of smell disappears, this can indicate a disease such as Alzheimer's or Parkinson's disease. However, unlike previously assumed, general degenerations in the nervous system do not play a leading role in the loss of the sense of smell with increasing age, but individual nerve cells or classes of nerves are decisive.
The finding 'opens up a whole new research area to look at neuroinflammation in the context of Alzheimer's and Parkinson's,' the lead researcher said. 'But the clinical impact will be in many, many different areas.'