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Memory Impairment in Alzheimer’s Caused By a Reduction of Activity in Brain Proteins

Research carried out by scientists at the University of Haifa has shed new light on the activity of the brain proteins that are associated with memory impairments in Alzheimer’s diseases. The study, which was published in the Journal of Neuroscience, also suggests that it is possible to ‘repair’ this activity and thus improve the memory of people with the disease.

Using mouse models of Alzheimer’s the researchers, led by research student Yifat Segev, discovered that when the nerve cells experience a certain type of metabolic stress, they reduce their activity level. However, as the stress is ongoing, it has a long term effect on cognitive functioning, as the cells never have the chance to return to normal function.

Previously undertaken research discovered a link

Earlier research into Alzheimer’s has put most of its focus on finding ways to combat the disease after it has started. However, the disease is already present in the brain long before symptoms appear. Prior to the current study, Segev has previously undertaken research to find a connection between a genetic condition already identified as a risk factor for Alzheimer’s and premature aging. As a result of this work, she discovered a link between the abnormal activity of a specific protein which regulates the formation of the new proteins which are essential for creating long-term memories, and a human gene which is known to be a key risk factor for sporadic Alzheimer’s.

Segev has used this new study to gain further understanding of this abnormal process, plus she also discovered that by repairing the process, it was possible to improve the ability to generate new memories. The mouse models exhibited signs of damage to their spatial memory, due to a change in the activity of the proteins. This led to an elevation of an additional protein, which affected the mice’s ability to make long-term memories. Furthermore, Segev found that cells that were under stress reduced their activity during the stressful period. However, as the stress is chronic, the cells never return to normal activity.
As a result of these findings, Segev hopes that we are one step closer to finding a drug that will be able to delay the onset of cognitive symptoms, not just in dementia patients, but for people suffering from other cognitive impairments.

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