Human beings are works in progress that mistakenly think they’re finished.” Dan Gilbert shares recent research on a phenomenon he calls the “end of history illusion,” where we somehow imagine that the person we are right now is the person we’ll be for the rest of time. Hint: that’s not the case.
Worldwide, there are at least 44 million people living with Alzheimer’s and other dementias. Everyone who has a brain is at risk to develop Alzheimer’s—but everyone can help to fight it.
Now is the time to get involved. Together we can end Alzheimer’s
A commonly prescribed antidepressant can reduce production of the main ingredient in Alzheimer’s brain plaques, according to new research at Washington University School of Medicine in St. Louis and the University of Pennsylvania.
The findings, in mice and people, are published May 14 in Science Translational Medicine. They support preliminary mouse studies that evaluated a variety of antidepressants.
Brain plaques are tied closely to memory problems and other cognitive impairments caused by Alzheimer’s disease. Stopping plaque buildup may halt the disastrous mental decline caused by the disorder.
The scientists found that the antidepressant citalopram stopped the growth of plaques in a mouse model of Alzheimer’s disease. And in young adults who were cognitively healthy, a single dose of the antidepressant lowered by 37 percent the production of amyloid beta, the primary ingredient in plaques.
Although the findings are encouraging, the scientists caution that it would be premature for people to take antidepressants solely to slow the development of Alzheimer’s disease.
“Antidepressants appear to be significantly reducing amyloid beta production, and that’s exciting,” said senior author John Cirrito, PhD, assistant professor of neurology at Washington University. “But while antidepressants generally are well tolerated, they have risks and side effects. Until we can more definitively prove that these drugs help slow or stop Alzheimer’s in humans, the risks aren’t worth it. There is still much more work to do.”
Amyloid beta is a protein produced by normal brain activity. Levels of this protein rise in the brains of patients with Alzheimer’s, causing it to clump together into plaques. Plaques also are sometimes present in cognitively normal brains.
Cirrito’s earlier research had shown that serotonin, a chemical messenger in the brain, reduces amyloid beta production. First author Yvette Sheline, MD, also has linked treatment with antidepressants to reduced plaque levels in cognitively healthy individuals.
Most antidepressants keep serotonin circulating in the brain, so this led Cirrito and Sheline to wonder whether the drugs block the increase of amyloid beta levels and slow the progression of Alzheimer’s.
In 2011, the researchers tested several antidepressants in young mice genetically altered to develop Alzheimer’s disease as they aged. In these mice, which had not yet developed brain plaques, antidepressants reduced amyloid beta production by an average of 25 percent after 24 hours.
For the new study, the team gave citalopram to older mice with brain plaques. Jin-Moo Lee, MD, PhD, professor of neurology, used a technique called two-photon imaging to track the growth of Alzheimer’s-like plaques in the mice for 28 days. Giving the mice the antidepressant stopped the growth of existing plaques and reduced the formation of new plaques by 78 percent.
In a second experiment, the scientists gave a single dose of citalopram to 23 people ages 18 to 50 who were not cognitively impaired or depressed. Samples of spinal fluid taken from the participants over the next 24 hours showed a 37 percent drop in amyloid beta production.
Now the researchers are trying to learn the molecular details of how serotonin affects amyloid beta production in mouse models.
“We also plan to study older adults who will be treated for two weeks with antidepressants,” said Sheline, who is now at the University of Pennsylvannia. “If we see a drop in levels of amyloid beta in their spinal fluid after two weeks, then we will know that this beneficial reduction in amyloid beta is sustainable.”
Several medications can help people with alcohol use disorders maintain abstinence or reduce drinking, according to research from the University of North Carolina at Chapel Hill.
The work, published today in the Journal of the American Medical Association (JAMA) and funded by the Agency for Healthcare Research and Quality (AHRQ), provides additional options for clinicians to effectively address this global concern.
Although alcohol use disorders are associated with many health problems, including cancers, stroke and depression, fewer than one-third of people with the disorders receive any treatment and less than 10 percent receive medications to help reduce alcohol consumption.
“There are many studies that have tried to show whether certain medications can help with alcohol use disorders, but it is a lot of information to digest and many providers do not know what works or doesn’t work,” said Daniel Jonas, lead author of the study and professor in the department of medicine and the Cecil G. Sheps Center for Health Services Research. ”When you synthesize all the evidence, it shows pretty clearly that some medications do work.”
Jonas led a team from the RTI-UNC Evidence-based Practice Center to review published studies examining the use of drugs to treat alcohol use disorders. The researchers conducted a systematic review of 122 randomized controlled trials and one cohort study. They then graded the strength of the evidence on the impact of drugs on alcohol consumption.
They found that two drugs, acamprosate (brand name Campral) and oral naltrexone (brand name Revia), have the best evidence supporting their benefits. Both drugs reduced return to drinking and improved other drinking outcomes. Among medications used off-label (i.e., those not FDA approved for alcohol use disorders), moderate evidence showed improvement in some drinking outcomes for topiramate and nalmefene.
“The health implications of preventing return to drinking and reducing alcohol consumption are substantial,” said Jonas. ”Modeling studies have shown that such improvements would result in significant reductions in alcohol-attributable mortality, costs from health care, arrests and motor vehicle accidents.”
“This work expands upon the growing evidence that medications can play a valuable role in the treatment of alcohol use disorders,” said James Garbutt, professor of psychiatry and scientist at UNC’s Bowles Center for Alcohol Studies and senior author on the paper. “We are hopeful that this information will encourage clinicians to strongly consider these medications and that individuals will gain awareness that there are medications that can help them to stop or significantly reduce their alcohol use.”
The study was developed by the AHRQ-funded RTI-UNC Evidence-based Practice Center is a collaboration between RTI International and the University of North Carolina at Chapel Hill. Jonas co-directs the center with Meera Viswanathan at RTI. The review is an update of the first product of the center, which was published in 1999 in JAMA. Since 1999, there has been more than a tenfold increase in the number of individuals studied in controlled clinical trials of naltrexone and acamprosate, and many trials of medications that are not FDA-approved.
