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A new study published in the journal Brain overturns thinking on the role of toxic peptides in the development of Alzheimer's disease. Sporadic Alzheimer's disease accounts for 99% of all Alzheimer's cases, and involves the development of toxic peptide deposits in the brain. These peptide deposits cause the neuronal networks to be destroyed, leading to disorientation, memory loss, changes in behavior and death. Although studies of Alzheimer's in animal models typically use mice with mutated human genes, the new study - conducted by researchers at the University of Oslo in Norway - used a new mouse model for the more common sporadic form of Alzheimer's. To create this new mouse model, the function was removed from two genes in the brain that are used to excrete and digest toxic Alzheimer's peptide beta-amyloid. The researchers say this new "transgene-free" mouse model allows studies to be conducted without "artificial overexpressi

Numerous studies have associated sleep with improved memory. But can sleep improve memory enough to help patients with Alzheimer's? This is what researchers from Washington University School of Medicine in St. Louis set out to investigate. Paul Shaw, PhD, professor of neurobiology at the Washington University School of Medicine, and colleagues conducted their study on three groups of fruit flies - whose brains regulate sleep in a similar way to humans. In each group of flies, the researchers disabled a gene to cause different memory problems, but all of which interfered with their ability to make new memories. In one group, the disabled gene triggered the development of a memory condition similar to Alzheimer's disease . Another group of flies had problems making brain connections that encode memories while another group had too many of these brain connections. Next, Shaw and colleagues increased the amount of sleep each group of flies got using one of three me

While nobody knows exactly what causes the complex brain changes that lead to Alzheimer's disease, scientists suspect one of the drivers is the accumulation of plaques of a faulty protein called beta-amyloid. Now, a new study of mice shows how too much sugar in the blood can speed up the production of the protein. Earlier studies have pointed to diabetes - where the body fails to control high blood sugar naturally with insulin - as a possible contributor to Alzheimer's disease , but the new study links high blood sugar itself to beta-amyloid. Researchers from the School of Medicine at Washington University in St. Louis (WUSTL) report their findings in The Journal of Clinical Investigation . Lead author and postdoctoral research scholar Dr. Shannon Macauley says: "Our results suggest that diabetes, or other conditions that make it hard to control blood sugar levels, can have harmful effects on brain function and exacerbate neurological conditions such

The University of Virginia claim that "decades of textbook teaching" have been overturned by their researchers, who have found a previously undiscovered connection between the brain and the immune system. Jonathan Kipnis, a professor in The University of Virginia's (UVa) Department of Neuroscience and director of UVa's Center for Brain Immunology and Glia, says his team's discovery "changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can't be studied. But now we can ask mechanistic questions." Not only is it surprising that the vessels connecting these two bodily systems have escaped detection for so long - when the lymphatic system has been so comprehensively studied - but the researchers say the discovery could have a huge impact on the study and treatment of neurological diseases such as autism , Alzheimer's disease and multiple sclerosis . "Instead of