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How to eliminate stress in Parkinson’s disease, a new way of thinking in schizophrenia or fear circuits are some of the matters of the mind that is the last issue of the prestigious journal Nature, Which dedicates its content to studies related to neurology.
The first study stated that the application of antihypertensive drugs can reduce cell death associated with Parkinson’s. The work, led by James Surmeier, a researcher at Northwestern University (USA), explains clearly why dopamine-secreting neurons in the substantia nigra are selectively removed during the disease process.
These are atypical and secreting neurons that generate rhythmic spontaneous electrical activity without the help of other cells. “But this innate motor activity creates oxidative stress in the mitochondria of cells,” said Surmeier.
The expulsion of the DJ-1, a gene associated with early stage Parkinson’s disease, oxidative stress increases selectively in these cells and stressed, which helps explain why these neurons die in particular.
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Clarified the mechanism by which mitochondria are transported within a few small cytoplasmic RNA necessary for the proper functioning of the ” powerhouse “of the cell
Mitochondria , of course, have their own genome , independent of nuclear , its expression is not autonomous and requires the support of some elements of the ” machinery ” phone. In particular needs to be transported inside the mitochondria several small cytoplasmic RNA . So far , however, were not yet clear at the underlying mechanisms of these RNAs in the powerhouse of the cell.
Now , a group of researchers at the University of California at Los Angeles explained how this happens and describes an article published in the journal Cell.
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A study group coordinated by the Cell Death Regulation of Biomedical Research Institute of Bellvitge (IDIBELL) found that glucose deprivation leads to self-destruction of tumor cells resistant to chemotherapy. The research is published in the online edition of the journal Cell Death and Differentiation. The study opens the door to new therapeutic strategies against cancer.
The appearance of a tumor is a complex process in which the cell acquires genetic or epigenetic alterations that confer advantages respect to normal cells because they reproduce rapidly, spread throughout the body and are resistant to natural mechanisms of programmed cell death (apoptosis). That is why so in a supportive environment, tumor cells are immortal.
Apoptosis or programmed cell death is a consequence of the activity chain proteins. This natural self-destructive process, necessary for the survival of the organism, begins in the mitochondria (energy-producing elements into the cells) by the action of a protein called Bax and Bak, the Bcl-2 family. Alterations in these proteins are common in cancer.
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The gene in question is called AFG3L2 and contains information for a protein involved in the metabolism of mitochondria, the power plants of our cells,
Identified the genetic defect responsible for a particular genetic form of ataxia, SCA28: to announce a study financed by Telethon and published online on the site Nature Genetics Franco Taroni, researcher of Neurologico Carlo Besta “in Milan, Marco Muzi-Falconi University of Milan and colleagues. The term ataxia is derived from the greek “disorder” and indicates a disorder of motor coordination that is often also associated with incontinence, difficulty swallowing and involuntary movements of limbs, trunk, head, eyes. The portion of the brain affected is the cerebellum, the control station of all voluntary movements of our body.
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Mitochondria are factories of cells: they give us the energy necessary for life. The defects may appear in the mitochondria are responsible for various human diseases such as neurodegenerative diseases, such as Parkinson’s or amyotrophic lateral sclerosis (ALS) [1]. About a thousand different proteins are mitochondria and fill each with a specific biological function related to its three-dimensional shape.
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