New Biomarker Predicts Alzheimer’s Disease and Link to Diabetes

 (Iowa State University) An enzyme found in the fluid around the brain and spine is giving researchers a snapshot of what happens inside the minds of Alzheimer’s patients and how that relates to cognitive decline.

Iowa State University researchers say higher levels of the enzyme, autotaxin, significantly predict memory impairment and Type 2 diabetes. Just a one-point difference in autotaxin levels – for example, going from a level of two to a three – is equal to a 3.5 to 5 times increase in the odds of being diagnosed with some form of memory loss, said Auriel Willette, an assistant professor of food science and human nutrition at Iowa State.

Autotaxin, often studied in cancer research, is an even stronger indicator of Type 2 diabetes. A single point increase reflects a 300 percent greater likelihood of having the disease or pre-diabetes. The results are published in the Journal of Alzheimer’s Disease. Willette and Kelsey McLimans, a graduate research assistant, say the discovery is important because of autotaxin’s proximity to the brain.

“We’ve been looking for metabolic biomarkers which are closer to the brain. We’re also looking for markers that reliably scale up with the disease and have consistently higher levels across the Alzheimer’s spectrum,” Willette said.

“This is as directly inside of the brain as we can get without taking a tissue biopsy.”

Willette’s previous research found a strong association between insulin resistance and memory decline and detrimental brain outcomes, increasing the risk for Alzheimer’s disease. Insulin resistance is a good indicator, but Willette says it has limitations because what happens in the body does not consistently translate to what happens in the brain. That is why the correlation with this new enzyme found in the cerebrospinal fluid is so important.

“It has a higher predictive rate for having Alzheimer’s disease,” McLimans said.

“We also found correlations with worse memory function, brain volume loss and the brain using less blood sugar, which have also been shown with insulin resistance, but autotaxin has a higher predictive value.”

Physical Health Linked to Memory

The fact that autotaxin is a strong predictor of Type 2 diabetes and memory decline emphasizes the importance of good physical health. Researchers say people with higher levels of autotaxin are more likely to be obese, which often causes an increase in insulin resistance.

Willette says autotaxin levels can determine the amount of energy the brain is using in areas affected by Alzheimer’s disease. People with higher autotaxin levels had fewer and smaller brain cells in the frontal and temporal lobes, areas of the brain associated with memory and executive function. As a result, they had lower scores for memory and tests related to reasoning and multitasking.

“Autotaxin is related to less real estate in the brain, and smaller brain regions in Alzheimer’s disease mean they are less able to carry out their functions,” Willette said.

“It’s the same thing with blood sugar. If the brain is using less blood sugar, neurons have less fuel and start making mistakes and in general do not process information as quickly.”

Researchers analyzed data from 287 adults collected through the Alzheimer’s Disease Neuroimaging Initiative, a public-private partnership working to determine whether MRI and PET scans as well as biological markers can measure the progression of cognitive impairment and Alzheimer’s disease. The data came from adults ranging in age from 56 to 89 years old. Study participants completed various tests to measure cognitive function. This included repeating a list of words over various time increments.

The research was supported by an Iowa State Presidential Initiative for Interdisciplinary Research grant and a National Institutes of Health grant.

Citation

http://www.news.iastate.edu/news/2016/12/19/alzheimersautotaxin

Journal Reference:

Kelsey E. McLimans, Auriel A. Willette. Autotaxin is Related to Metabolic Dysfunction and Predicts Alzheimer’s Disease Outcomes. Journal of Alzheimer’s Disease, December 2016

Copyright © 1995-2016, Iowa State University of Science and Technology. All rights reserved.

 

Single Protein May Hold Secret to Treating Parkinson’s Disease and More

(Gladstone Institutes) A new way to regulate protein levels and functions could be the answer to treating devastating neurological conditions.

New details learned about a key cellular protein could lead to treatments for neurodegenerative diseases, such as Parkinson’s, Huntington’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS).

At their root, these disorders are triggered by misbehaving proteins in the brain. The proteins misfold and accumulate in neurons, inflicting damage and eventually killing the cells. In a new study, researchers in the laboratory of Steven Finkbeiner, MD, PhD, at the Gladstone Institutes used a different protein, Nrf2, to restore levels of the disease-causing proteins to a normal, healthy range, thereby preventing cell death.

The researchers tested Nrf2 in two models of Parkinson’s disease: cells with mutations in the proteins LRRK2 and α-synuclein. By activating Nrf2, the researchers turned on several “house-cleaning” mechanisms in the cell to remove excess LRRK2 and α-synuclein.

“Nrf2 coordinates a whole program of gene expression, but we didn’t know how important it was for regulating protein levels until now,” explained first author Gaia Skibinski, PhD, a staff research scientist at Gladstone.

“Overexpressing Nrf2 in cellular models of Parkinson’s disease resulted in a huge effect. In fact, it protects cells against the disease better than anything else we’ve found.”

In the study, published in the Proceedings of the National Academy of Sciences, the scientists used both rat neurons and human neurons created from induced pluripotent stem cells. They then programmed the neurons to express Nrf2 and either mutant LRRK2 or α-synuclein. Using a one-of-a-kind robotic microscope developed by the Finkbeiner laboratory, the researchers tagged and tracked individual neurons over time to monitor their protein levels and overall health. They took thousands of images of the cells over the course of a week, measuring the development and demise of each one.

The scientists discovered that Nrf2 worked in different ways to help remove either mutant LRRK2 or α-synuclein from the cells. For mutant LRRK2, Nrf2 drove the protein to gather into incidental clumps that can remain in the cell without damaging it. For α-synuclein, Nrf2 accelerated the breakdown and clearance of the protein, reducing its levels in the cell.

“I am very enthusiastic about this strategy for treating neurodegenerative diseases,” said Finkbeiner, a senior investigator at Gladstone and senior author on the paper.

“We’ve tested Nrf2 in models of Huntington’s disease, Parkinson’s disease, and ALS, and it is the most protective thing we’ve ever found. Based on the magnitude and the breadth of the effect, we really want to understand Nrf2 and its role in protein regulation better.”

The scientists say that Nrf2 itself may be difficult to target with a drug because it is involved in so many cellular processes, so they are now focusing on some of its downstream effects. They hope to identify other players in the protein regulation pathway that interact with Nrf2 to improve cell health and that may be easier to drug.

Funding was provided by the National Institutes of Mental Health, National Institute of Neurological Disorders and Stroke, National Human Genome Research Institute, California Institute of Regenerative Medicine, Taube/Koret Center, Michael J. Fox Foundation, ALS Association, National Center for Research Resources, and the Betty Brown family. The work is dedicated to the memory of Nita Hirsch.

Citation

https://www.eurekalert.org/pub_releases/2016-12/gi-spm122016.php

Copyright © 2016 by the American Association for the Advancement of Science (AAAS)

 

“Sniff Test” May Be Useful in Diagnosing Early Alzheimer’s Disease

(Journal of Alzheimer’s Disease) Tests that measure the sense of smell may soon become common in neurologists’ offices. Scientists have been finding increasing evidence that the sense of smell declines sharply in the early stages of Alzheimer’s, and now a new study from the Perelman School of Medicine at the University of Pennsylvania published today in the Journal of Alzheimer’s Disease confirms that administering a simple “sniff test” can enhance the accuracy of diagnosing this dreaded disease.

The sniff test also appears to be useful for diagnosing a pre-dementia condition called mild cognitive impairment (MCI), which often progresses to Alzheimer’s dementia within a few years.

Neurologists have been eager to find new ways to identify people who are at high risk of Alzheimer’s dementia but do not yet show any symptoms. There is a widespread consensus that Alzheimer’s medications now under development may not work after dementia has set in.

“There’s the exciting possibility here that a decline in the sense of smell can be used to identify people at risk years before they develop dementia,” said principal investigator David R. Roalf, PhD, an assistant professor in the department of Psychiatry at Penn.

Roalf and his colleagues used a simple, commercially available test known as the Sniffin’ Sticks Odor Identification Test, in which subjects must try to identify 16 different odors. They administered the sniff test, and a standard cognitive test (the Montreal Cognitive Assessment), to 728 elderly people.

The subjects had already been evaluated by doctors at Penn with an array of neurological methods, and according to expert consensus had been placed in one of three categories: “healthy older adult,” “mild cognitive impairment,” or “Alzheimer’s dementia.” Roalf and his team used the results from the cognitive test alone, or combined with the sniff test, to see how well they identified subjects in each category.

As researchers report, the sniff test added significantly to diagnostic accuracy when combined with the cognitive test.

For example, the cognitive test alone correctly classified only 75 percent of people with MCI, but that figure rose to 87 percent when the sniff test results were added. Combining the two tests also enabled more accurate identification of healthy older adults and those with Alzheimer’s dementia. The combination even boosted accuracy in assigning people to milder or more advanced categories of MCI.

“These results suggest that a simple odor identification test can be a useful supplementary tool for clinically categorizing MCI and Alzheimer’s, and even for identifying people who are at the highest risk of worsening,” Roalf said.

Prompted by prior studies that have linked a weakening sense of smell to Alzheimer’s, doctors in a few larger dementia clinics already have begun to use smell tests in their assessments of elderly patients. Part of the reason the practice has not yet become common is that the tests that seem most useful take too long to administer. Roalf and colleagues are now trying to develop a briefer test that works as well as the longer ones.

“We’re hoping to shorten the Sniffin’ Sticks test, which normally takes 5 to 8 minutes, down to 3 minutes or so, and validate that shorter test’s usefulness in diagnosing MCI and dementia—we think that will encourage more neurology clinics to do this type of screening,” Roalf said.

Roalf and his laboratory also plan to investigate whether protein markers of Alzheimer’s, which are present in the olfactory region of the brain before dementia occurs, can be detected in nasal fluid to provide an even earlier warning of the disease process.

Studies suggest that a high proportion of older adults who have cognitive impairment are not identified as such, in part due to lack of adequate screening.

The study’s first author was Penn’s Megan Quarmley; the other co-authors were Paul J. Moberg, Dawn Mechanic-Hamilton, Sushila Kabadi, and David A. Wolk, all of Penn, and Steven E. Arnold of Harvard University and Massachusetts General Hospital.

Funding was provided by the National Institute of Mental Health (K01 497 MH102609), National Institute on Aging (P30 AG10124), and the Penn Center of Excellence for Research on Neurodegenerative Diseases.

Citation

http://www.j-alz.com/content/penn-study-confirms-%E2%80%9Csniff-test%E2%80%9D-may-be-useful-diagnosing-early-alzheimer%E2%80%99s-disease

Source:

Quarmley M, Moberg PJ, Mechanic-Hamilton D, Kabadi S, Arnold SE, Wolk DA, Roalf DR. Odor Identification Screening Improves Diagnostic Classification in Incipient Alzheimer’s Disease. J Alzheimers Dis. 2016 Nov 18.

Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2016

 

Occupational Therapy May Have Potential to Slow Down Decline and Reduce Behavioral Troubles in Dementia Patients

(Journal of Alzheimer’s Disease) A French observational study in real life showed that dementia patients benefiting from occupational therapy sessions report relevant clinical benefits over the intervention period, according to a research study published in the Journal of Alzheimer’s Disease this month.

The research suggested the influence of occupational therapy on reducing behavioral troubles, caregivers’ burden and amount of informal care over the intervention period and a stabilization over the 3-months period thereafter.

France put a massive effort for improving dementia care through a national Alzheimer plan in 2008 and this effort was confirmed by the next government (Neurodegenerative Diseases Plan 2014-2019). Some new care models and interventions have been implemented such as integrated care, case management or occupational therapy.

Occupational therapy has been spread nationwide through specialized Alzheimer team intervening at home with medical prescription. Even if efficacy of occupational therapy has been demonstrated in some clinical trials, its efficacy under routine care conditions was unknown and deserved to be investigated.

The research was conducted on a network of 16 specialized Alzheimer team in Aquitaine, South West of France and was supported by the regional agency of Health (Agence Régionale de la Santé d’Aquitaine). Titled “Benefits of Occupational Therapy in Dementia Patients: Findings from a Real-World Observational Study,” the study included 421 dementia patient who had been referred to occupational therapy by their general practionner or memory clinics and who had been followed up to 6 months. Research studied the clinical evolution of patients between inclusion and 3 month follow-up (end of the 15 home sessions) and between 3 and 6-month follow-up (no session planned over this timeframe).

The study’s results indicate that behavioral troubles, caregivers’ burden, amount of informal care provided by caregivers and patients’ quality of life were significantly reduced over the 3-month intervention period and remained stable thereafter.

Cognitive performances remained stable over the 6-month study period and functional performances remained stable over the 3-month intervention period but were significantly reduced thereafter.

Moreover, patients who had been diagnosed more recently and those with milder cognitive deficits may gain more benefits from occupational therapy in terms of functional decline or caregivers’ burden decline. These findings suggest that occupational therapy should target early dementia stages in order to optimize its potential clinical benefits.

In many Western countries, recent national guidelines have aimed at improving home dementia care. This study highlights the potential occupational therapy in terms of patients’ and their caregivers’ well-being.

The findings also opens a new field of research on occupational therapy. Indeed, occupational therapy has been conceptualized as a short-term home intervention, but long-term benefits and consequences of disruption are unknown.

“Future studies should explore more in detail which sub-groups of patients could gain more benefits from OT as well as its long-term clinical effects notably on global care quality and users’ satisfaction” stated Clément Pimouguet.

Moreover, strategies aiming to improve initial benefits of occupational therapy should be promoted. The French research team will conduct a randomized trial that aim to compare the maintenance of occupational therapy over an additional 4-month period and usual occupation therapy as recommended.

Citation

http://www.j-alz.com/content/occupational-therapy-may-have-potential-slow-down-functional-decline-and-reduce-behavioral

Source:

Pimouguet C, Le Goff M, Wittwer J, Dartigues JF, Helmer C. Benefits of Occupational Therapy in Dementia Patients: Findings from a Real-World Observational Study. J Alzheimers Dis. 2016 Dec 9, doi: 10.3233/JAD-160820.

Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2016

 

Early Signs of Alzheimer’s Disease in Cerebrospinal Fluid

(German Center for Neurodegenerative Disease) Immune cells of the brain become active years before the disease becomes apparent.

Little is known about the role of the brain’s immune system in Alzheimer’s disease. Researchers at the Munich site of the German Center for Neurodegenerative Diseases (DZNE) and the hospital of the Ludwig Maximilian University (LMU) Munich have now found an early immune response in individuals with a genetic predisposition to Alzheimer’s: their brain’s showed abnormal immune reactions as early as about seven years before the expected onset of dementia.

These results demonstrate that in cases of Alzheimer’s, inflammatory processes in the brain evolve dynamically and are precursors of dementia. These immune responses can be detected by means of a protein in the cerebrospinal fluid, offering physicians the possibility to trace the progression of the disease. The study results are published in the journal Science Translational Medicine.

The scientists headed by Prof. Christian Haass and Prof. Michael Ewers were able to detect an increasing immune activity of the brain by measuring levels of the protein “TREM2” in the cerebrospinal fluid. TREM2 is segregated by certain immune cells of the brain – called microglia – and thus reflects their activity. In cases of the inherited form of Alzheimer’s disease, the timing for the onset of dementia can be precisely predicted. The researchers were therefore able to monitor the rise of TREM2 levels years before the expected occurrence of dementia symptoms.

“The activity of the microglia is stimulated by dying brain cells, not by the deposits of amyloid proteins, called plaques, which also occur in Alzheimer’s disease,” Haass notes.

“The microglia may have a protective function, which however comes to a standstill as the disease progresses. We are therefore searching for drugs to increase the activity of the microglia.”

Part of the DIAN project

127 individuals with a genetic predisposition to Alzheimer’s participated in the study. They were on average 40 years old. The vast majority showed no symptoms of dementia or had only minor cognitive impairments. The study was conducted as part of the so-called DIAN project (Dominantly Inherited Alzheimer Network), a worldwide network for research into the inherited form of Alzheimer’s disease.

According to Ewers,

“There are many similarities between the inherited form of Alzheimer’s disease and the so-called sporadic variant, which is far more common. TREM2 levels could therefore be a biomarker used to track immune activity while Alzheimer’s is progressing, irrespective of whether the disease is genetic or not. TREM2 may also serve as a therapeutic marker to monitor drug response. We will look into these aspects in the future.

 

Citation

http://www.en.uni-muenchen.de/news/newsarchiv/2016/haass_ewers_trem2.html

Article: Early changes in CSF sTREM2 in dominantly inherited Alzheimer’s disease occur after amyloid deposition and neuronal injury, Marc Suárez-Calvet, Miguel Angel Araque Caballero, Gernot Kleinberger, Randall J. Bateman, Anne M. Fagan, John C. Morris, Johannes Levin, Adrian Danek, Michael Ewers, Christian Haass, Science Translational Medicine, doi: 10.1126/scitranslmed.aag1767, published 14 December 2016.

Copyright Ludwig Maximilian University

 

Antipsychotic Drug Use Increases Risk of Mortality with Alzheimer’s Disease

(Journal of Alzheimer’s Disease) Antipsychotic drug use is associated with a 60 percent increased risk of mortality among persons with Alzheimer’s disease, shows a recent study from the University of Eastern Finland. The risk was highest at the beginning of drug use and remained increased in long-term use. Use of two or more antipsychotic drugs concomitantly was associated with almost two times higher risk of mortality than monotherapy. The results were published in the Journal of Alzheimer’s Disease.

The study compared the risk of mortality between the most commonly used antipsychotic drugs. Haloperidol was associated with highest risk of mortality, and the use of higher doses of haloperidol and risperidone were associated with an increased risk of mortality compared with low-dose risperidone use.

The association of antipsychotic drug use with mortality was investigated in the Finnish nationwide MEDALZ study including community-dwelling persons diagnosed with Alzheimer’s disease between 2005 and 2011. Of 57,755 persons, 27% started antipsychotic drug use during the follow-up. The register-based study was restricted to persons who did not use antipsychotics during the year preceding the start of follow-up, did not have history of a psychiatric disorder, and did not have active cancer at the start of follow-up.

The results of this study are in line with many previous studies. The first warnings of an increased risk of mortality among antipsychotic users were issued over 10 years ago. This study provides new knowledge on the risk of mortality during long-term use and during concomitant use of two or more antipsychotic drugs.

The study confirms current recommendations that antipsychotic drugs should be used only for the most difficult behavioural symptoms of dementia, such as agitation and aggression, and the duration of use should be limited. Furthermore, the lowest effective doses are recommended, and concomitant use of two or more antipsychotics should be avoided.

 

 

Protein in Urine Linked to Increased Risk of Memory Problems, Dementia

(American Academy of Neurology)People who have protein in their urine, which is a sign of kidney problems, may also be more likely to later develop problems with thinking and memory skills or even dementia, according to a meta-analysis published in the December 14, 2016, online issue of Neurology, the medical journal of the American Academy of Neurology.

The researchers looked at all available studies on kidney problems and the development of cognitive impairment or dementia.

“Kidney dysfunction has been considered a possible risk factor for cognitive impairment or dementia,” said Kay Deckers, MSc, of Maastricht University in the Netherlands, author of the systematic review and meta-analysis.

“Chronic kidney disease and dementia share many risk factors, such as high blood pressure, diabetes and high cholesterol, and both show similar effects on the brain, so they may have shared vascular factors or there may even be a direct effect on the brain from kidney problems.”

A total of 22 studies on the topic were included in the systematic review. Five of the studies, including 27,805 people, were evaluated in the meta-analysis on protein in the urine, also called albuminuria or proteinuria. The analysis showed that people with protein in the urine were 35 percent more likely to develop cognitive impairment or dementia than people who did not have protein in their urine.

For another marker of kidney function, estimated glomerular filtration rate, the results were mixed and did not show an association. For three other markers of kidney function, cystatin C, serum creatinine and creatinine clearance, no meta-analysis could be completed because the few studies available did not use the same methods and could not be compared.

“Protein in the urine was associated with a modestly increased risk of cognitive impairment or dementia,” Deckers said.

“More research is needed to determine whether the kidney problems are a cause of the cognitive problems or if they are both caused by the same mechanisms.”

The study was supported by the In-MINDD (Innovative Midlife Intervention for Dementia Deterrence) project funded by the European Union’s Framework Program Seven.

To learn more about the brain, visit www.aan.com/patients.

Citation

https://www.aan.com/PressRoom/Home/PressRelease/1507

Journal Reference:

Kay Deckers, Ileana Camerino, Martin P.J. van Boxtel, Frans R.J. Verhey, Kate Irving, Carol Brayne, Miia Kivipelto, John M. Starr, Kristine Yaffe, Peter W. de Leeuw, and Sebastian Köhler. Dementia risk in renal dysfunction: A systematic review and meta-analysis of prospective studies. Neurology, December 2016 DOI: 10.1212/WNL.0000000000003482%0D

©2016 American Academy of Neurology – All Rights Reserved

 

Cholesterol-Fighting Drugs Lower Risk of Alzheimer’s Disease

(University of Southern California) The incidence of Alzheimer’s was reduced for beneficiaries frequently prescribed statins (high users), compared to low users, researchers find.

Common anti-cholesterol drugs show promise for reducing the risk of Alzheimer’s disease, a University of Southern California-led study of Medicare data reveals.

The new study shows that, based on a sample of 399,979 Medicare beneficiaries, men and women who took statins two years or more lowered their risk of Alzheimer’s disease in the period spanning from 2009 to 2013.

The incidence of Alzheimer’s disease was reduced for beneficiaries frequently prescribed statins (high users), compared to low users, USC and University of Arizona researchers found. Among women who were high users, the incidence rate was 15 percent lower. Among men, the rate was 12 percent lower.

Researchers noted that black men were the only group that did not show a statistically significant reduction in risk, likely due to sample size.

“We may not need to wait for a cure to make a difference for patients currently at risk of the disease. Existing drugs, alone or in combination, may affect Alzheimer’s risk,” said lead and corresponding author Julie Zissimopoulos, associate director of the USC Leonard D. Schaeffer Center for Health Policy and Economics and assistant professor at USC Price School of Public Policy.

Prior studies have shown a link between cholesterol and the hallmark of Alzheimer’s disease: the beta-amyloid plaques that interfere with memory and other brain functions.

“We looked to statins as a candidate because they are widely used and have resulted in the reduction of cholesterol,” she said.

The findings were published on Dec. 12 in JAMA Neurology.

Urgent Need for Treatement

Although much is known about Alzheimer’s, scientists have been unsuccessful so far in developing effective treatments to prevent and slow the memory-erasing disease that affects more than 5 million Americans. Hopes were high for the experimental drug, solanezumab, by Eli Lilly that was designed to attack the amyloid plaques. The drug failed for patients with mild dementia in a recent large clinical trial.

“Beta-amyloid continues to be a therapeutic target; however, once a patient is symptomatic and has the plaques, it may be too late,” said Zissimopoulos.

“Some researchers believe successful treatment may involve a ‘cocktail’ of several medications aimed at multiple targets.”

Age-related diseases are among the intractable problems that USC researchers in multiple disciplines are seeking to unravel. Efforts to understand Alzheimer’s and dementia and to find preventive interventions and precise treatments are much more pressing as the baby boomer generation ages.

In a previous study, Zissimopoulos found that if medical advances could delay the disease’s onset by a year, more than 2 million Americans would be spared from developing Alzheimer’s. This also would result in a $220 billion savings in health and caregiving costs by 2050.

Zissimopoulos cautioned that a silver tsunami of aging baby boomers will increase the number of Alzheimer’s patients 70 and older to 9.1 million by 2050. Annual health care costs will surge to $1.5 trillion.

High Users vs. Low Users

Other studies have compared statin users to non-statin users with a range of health statuses. However, Zissimopoulos said the USC-led team focused only on statin users.

The research team divided the patients into two groups: high-use beneficiaries — those who took statins for two years or more between 2006 and 2008 — and low-use beneficiaries who took them less frequently or who started taking statins after 2008. Both sets of beneficiaries were in similar health and had no diagnosis of Alzheimer’s disease. The researchers studied records dating from 2009 to 2013 to track the onset of Alzheimer’s disease.

The estimated 400,000 Medicare beneficiaries who became the focus of the study were 65 and older as of January 2006 and were continuously enrolled in Medicare fee-for-service and Part D prescription drug coverage. The study sought results on four of the most commonly prescribed statins: simvastatin, atorvastatin, pravastatin and rosuvastatin.

The researchers also found a reduction in risk for certain demographic groups who were frequently prescribed statins for two years or more.

The greatest drop in incidence of Alzheimer’s disease — 29 percent — was among Hispanic men. Among white men, high users of statins had an 11-percent lower risk of incidence of the disease. A similar reduction in risk — 12-percent — was found among Hispanic women.

The risk of Alzheimer’s disease was also lower for white women who were high users (15 percent lower than women who took statins less frequently).

Disease Risk by Statin

Simvastatin was linked to a reduced risk of Alzheimer’s for white women, Hispanic women and black women, as well as for white men and Hispanic men. Atrovastatin was associated with a reduced risk of Alzheimer’s for white women, Hispanic women, black women and Hispanic men.

Pravastatin and rosuvastatin results showed a statistically significant reduction of Alzheimer’s risk for only white women.

Some scientists believe that certain statins such as atorvastatin and simvastatin, known as lipophilics, would be most effective as an Alzheimer’s preventive treatment because they cross the blood-brain barrier, a protective layer of cells that restricts the types of substances that can pass to the brain.

“We generally found that they’re all associated with reduced risk,” Zissimopoulos said.

The researchers plan to study combinations of other existing drugs to measure their effects on the risk of Alzheimer’s disease.

“Anti-diabetic drugs have been linked to lower incidence of Alzheimer’s disease, as have some anti-hypertensives,” study co-author Geoffrey Joyce, director of health policy for the USC Schaeffer Center and an associate professor of the USC School of Pharmacy.

“But there is mixed evidence across the cardiovascular drug classes.”

The study was supported with a grant from the National Institute on Aging of the National Institutes of Health and the USC Zumberge Research Fund.

Study co-authors were Douglas Barthold of the USC Schaeffer Center and Roberta Diaz Brinton, formerly of the USC School of Pharmacy and now with the University of Arizona.

Citation

Cholesterol-fighting drugs lower risk of Alzheimer’s disease


By Emily Gersema

Journal Reference:

Julie M. Zissimopoulos, Douglas Barthold, Roberta Diaz Brinton, Geoffrey Joyce. Sex and Race Differences in the Association Between Statin Use and the Incidence of Alzheimer Disease. JAMA Neurology, 2016; DOI: 10.1001/jamaneurol.2016.3783

Copyright 2016 University of Southern California