Medication taken by patients who have had organ transplants to prevent organ rejection could also protect against the development of Alzheimer's disease, a new study has found.
Researchers from The University of Texas Medical Branch (UTMB) at Galveston analyzed the medical records of patients who received organ transplants, for whom any evidence of cognitive impairment or dementia is recorded and monitored. Their findings are published in the Journal of Alzheimer's Disease.
Alzheimer's disease is an age-associated neurodegenerative disorder and the sixth leading cause of death in the US. According to the Alzheimer's Association, of the top 10 causes of death in the country, it is the only one that cannot currently be prevented, cured or slowed.
Previously, scientists have found evidence suggesting that toxic protein clusters called beta-amyloid oligomers could be behind the memory impairment experienced by people with Alzheimer's disease, by specifically targeting and disrupting points of communication between brain cells.
The researchers from UTMB have previously demonstrated that the enzyme calcineurin - a regulator of communication between brain cells - is strongly associated with the toxic effects of beta-amyloid oligomers. Elevated levels of calcineurin are found in the nervous systems of people with Alzheimer's disease.
While studies in mice have shown that blocking calcineurin can restore memory function, suggesting that this could be a strategy for preventing Alzheimer's, it is a problematic approach to investigate as treatment with calcineurin-inhibiting agents also weakens the body's immune system.
The team was able to get around this problem by analyzing data for patients who had received organ transplants and were taking calcineurin inhibitor-based medication to prevention organ rejection. Such medication must be taken daily for the rest of the patients' lives.
Medical records were available for 2,644 patients. These participants were then separated into groups according to their age at the time of last visit or death, their ethnicity and their gender.
'Alzheimer's disease significantly less prevalent among transplant patients'
Of the 2,644 patients, eight exhibited signs of dementia. Two were younger than 65, five were aged from 65-74 and one was aged between 75-84.
The researchers then compared their findings with data obtained for age-matched patients from the 2014 Alzheimer's Association Facts and Figures dataset in order to compare the prevalence of the disease between the study participants and the general population.
"These data clearly show that the prevalence of dementia and Alzheimer's in our transplant patient group is significantly lower, in fact almost absent, when compared to national data from the general population," reports senior author Luca Cicalese.
While 11% of the general population of patients over 65 years had dementia, only 1.02% of the study subjects of the same age had the disease. Similarly, 15.3% of the American population over 75 years had Alzheimer's compared with only 0.6% of the study participants.
The majority of the study participants come from the state of Texas. Accordingly, the researchers compared their findings with the rates of prevalence in the state's general population and again found a disparity.
"Taken together, our findings from these people confirm the data obtained with animal models and support, for the first time in human subjects, our notion that calcineurin inhibition has a protective effect on the development and possible progression and even reversal of Alzheimer's disease," says senior author Giulio Taglialatela.
Prof. Taglialatela, director of UTMB's Mitchell Center for Neurodegenerative Diseases, states that the team is now working on devising treatment strategies to obtain the same beneficial effects in people with Alzheimer's disease with low doses of calcineurin inhibitors that minimize or avoid suppression of the immune system.
Previously, Medical News Today reported on a mouse study that suggested there may be a way to block the production of beta-amyloid protein.