Two experimental drugs that may treat Alzheimer’s disease also have broader, anti-aging properties that may reverse age-related cognitive decline. The drugs were tested on 9-month-old mice, which is equivalent to middle age for humans.
New research on mice is shedding light on how the aging process contributes to Alzheimer’s. Family history, genes, and some lifestyle choices can all influence a person’s likelihood of getting the disease. However, the biggest number of patients are as a result of age-related issues. Most people who receive Alzheimer’s diagnoses are over 65 years.
Research has shown that people aged 65 and above odds of developing the disease doubles every five years. However, scientists do not fully understand the actual underlying cause of this disease. Previous research has successfully shown that just before the onset of Alzheimer’s, there is always a faulty glucose metabolism, which leads to reduced brain functions and memory loss.
Researchers from Salk Institute for Biological Studies and the Scripps Research Institute — both in La Jolla, California, armed with this knowledge, set out to test several drugs that mimic age-related problems on mice.
Testing Alzheimer’s drug on mice
Curtis and his team also tested two experimental drugs CMS121 and J147. The two drugs had shown in previous studies to be neuroprotective in mouse models of Alzheimer’s with the possibility of reversing the disease.
Researchers fed the two compounds to mice aged nine months, which is equivalent to middle age for humans. After four months of taking these compounds, the researchers tested the behaviors and memory of the rodents’ brains. They also tested genetic changes that might have occurred during this period. The results were compared with tests from other rodents the same age, which was not going through the treatment.
Better cognitive abilities after treatment
The research found that mice that received this treatment had better cognitive abilities than their counterparts. The genes responsible for keeping mitochondrial active continued to be expressed through the aging process of the mice that took the treatment.
This was not the case for other rodents that did not receive treatment. This was possible because mice that received the compounds had an increase in levels of acetyl-coenzyme A.
The research confirmed that Alzheimer’s disease is a result of mitochondrial failure. The results also gave hope that this can be corrected in the future using similar compounds to treat Alzheimer’s. The compounds were also found to be anti-aging by maintaining high levels of mitochondrial activities.
If you know anyone who is suffering from this disease, seek help through getting connected to professional organizations and support groups.
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