In Alzheimer's disease sufferers, a new class of drugs has proved to be effective in preventing early memory loss, finds research.
In Alzheimer's disease sufferers, a new class of drugs has proved to be effective in preventing early memory loss, finds research. The small molecules, called MW108, stopped loss of memory and fixed damaged communication among brain cells in a mouse model of Alzheimer.
D. Martin Watterson, lead author of a paper on the study and the John G. Searle Professor of Molecular Biology and Biochemistry at Northwestern University Feinberg School of Medicine said that it is possible that someday this class of drugs could be given early on to people to arrest certain aspects of Alzheimer's.
Linda Van Eldik, a senior author of the paper and director of the University of Kentucky Sanders-Brown Center on Aging, said that these drugs can be beneficial when the nerve cells are just beginning to get damaged.
The novel drug-like molecule reduced activity of an enzyme that is over-activated during Alzheimer's and is considered a contributor to brain inflammation and impaired neuron function.
Strong communication between neurons in the brain is an essential process for memory formation.
The compound strikes at a new, single target that has long flown under the radar in Alzheimer 's drug development. The target is a stress-related protein kinase, p38alpha MAPK.
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In a key memory experiment in the study, mice brains were injected with beta-amyloid, whose increase is one hallmark of Alzheimer's in humans. One group of mice was then administered MW108 and another group was administered a placebo.
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The mice administered MW108 found the resting platform in the water maze as quickly as a control group of mice. The mice given the placebo made more mistakes and took longer to find the platform. They also had difficulty learning the location of the resting platform during the teaching phase.
Van Eldik said that the results show the compound prevented the cognitive impairment.
The study has been published in the journal PLOS ONE.
Source-ANI