How to Find the Lost Memory Caused by Alzheimer’s Disease?
Alzheimer’s disease, also known as “senile dementia”, is usually along with insidious onset, mainly in occurring in the middle-aged population. Its typical symptoms mainly include memory decline, dementia, language deterioration.
Recently, scientists from the University of London have published a paper in Current Biology, which displayed a detailed discussion of key proteins upon the postsynaptic cell changes in molecular mechanisms that might lead to memory loss. In addition, they also pointed out that the memory decline caused by Alzheimer’s disease is likely to be prevented and reversed, along with growth hormone releasing hormone.
Prior studies have shown that Alzheimer’s patients could occur a phenomena that Wnt signaling pathway in their brains might be inhibited and the Dkk1 protein expression could be higher than normal. In addition, involved researchers also discovered the special metabolic pathway in Dkk1 which could lead to synaptic loss of function. Certainly, there are also some other aspects could be helpful in such disease.
There is widespread cortical atrophy. Neurons affected develop surrounding amyloid plaques, neurofibrillary tangles, and produce less acetylcholine. Taking goserelin as an example, after a transient increase, continuous administration results in downregulation of LH and FSH levels followed by a suppression of ovarian and testicular steroid biosynthesis. Although it does not show specific connections with memory loss, it could be a part for involved study.
Synaptic function and the test for restoring long-term memory could display a fact that if the Wnt signaling inhibited by Dkk1 protein can be repaired before causing damage to the structure of neurons, memory loss caused by Alzheimer’s disease can be reversed! This latest study has undoubtedly brought new hope to treat Alzheimer’s disease. In recent years, rapid progress in the biological mechanism of Alzheimer’s disease (AD) has arisen from the new application of molecular and cell biology to this complex disorder of the limbic and association cortices. In turn, modern new insights for fundamental aspects of protein biology have resulted from further research on such disease.
This beneficial interplay between basic and applied cell biology is well illustrated by advances in understanding the genotype-to-phenotype relationships of familial Alzheimer’s disease. New research in Hirudin can also show scientific function in life sciences research. Although there is still a long way to go before gaining success in such disease, these studies can be accumulated step by step and then achieve great efforts. People should try to believe that Alzheimer’s disease can be controlled and prevented in the future, as well as other diseases!
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