Insomnia May Forecast Depression, Thinking Problems in Older People

Insomnia may significantly increase the risk that older adults will be unable to shake off depression, researchers say.

For the study, the investigators analyzed data on nearly 600 people over age 60 who visited primary care centers in New York City, Philadelphia and Pittsburgh. All had some level of depression.

Compared to patients whose sleep improved, those with worsening sleep problems were about 28 times more likely to be diagnosed with major depression at the end of the 12-month study.

Patients whose sleep worsened also had nearly 12 times the odds of minor depression and were 10% more likely to report having suicidal thoughts, according to the Johns Hopkins Bloomberg School of Public Health study.

The report was recently published online in the journal Sleep.

Compared to patients whose sleep improved, those with persistent, but not worsening, insomnia were more likely to have lasting depression. But their risk was not as high as patients whose sleep got worse.

“These results suggest that, among older adults with depression, insomnia symptoms offer an important clue to their risks for persistent depression and suicidal ideation,” said study senior author Adam Spira, a professor of mental health at Johns Hopkins in Baltimore.

“We can’t say that the sleep disturbances we’re seeing are necessarily causing the poor depression outcomes,” he said in a Hopkins news release. “But the results suggest that older adults who are being treated for depression and whose sleep problems are persistent or worsening need further clinical attention.”

Spira said the findings also suggest that treatment of sleep problems should be explored as a way to improve depression symptoms in older adults, as well as poor mental and health outcomes related to disturbed sleep.

Source: HealthDay

Maintaining Heart Health May Protect Against Cognitive Decline

People with a higher risk of developing cardiovascular disease have increased cognitive decline, including an increase in typical markers of Alzheimer’s disease, suggesting that monitoring and controlling for heart disease may be key to maintaining and improving cognitive health later in life, according to research published today in the Journal of the American College of Cardiology.

Dementia is a public health challenge, with 50 million people affected in 2017 and the World Health Organization predicting 82 million people by 2030. There is not currently an effective treatment for dementia, so identifying modifiable risk factors that could delay or prevent dementia onset are becoming more prominent.

Previous studies have reported how cardiovascular disease risk factors were related to smaller volumes of specific brain regions, such as white matter, gray matter and hippocampus, but findings have been inconsistent. Researchers in this study sought to compare Framingham General Cardiovascular Risk Scores (FGCRS), which incorporate demographic information with traditional cardiovascular risk factors to assess future risk, to an individual’s long-term decline in global and domain specific cognitive function.

Researchers followed 1,588 dementia-free participants from the Rush Memory and Aging Project for 21 years. The average age was 79.5 years. Their FGCRS was assessed at baseline and categorized into lowest, middle and highest groups according to heart disease risk. Each year participants’ episodic memory (memory of everyday events), semantic memory (long-term memory), working memory (short-term memory), visuospatial ability (capacity to identify visual and spatial relationships among objects) and perceptual speed (ability to accurately and completely compare letters, numbers, objects, pictures or patterns) was assessed using 19 tests to derive a composite score.

At the end of the study period, researchers found that having a higher cardiovascular risk burden was associated with faster decline in episodic memory, working memory and perceptual speed. Researchers also looked at MRI data for a subset of patients and found that higher FGCRS was associated with smaller volumes of hippocampus, cortical gray matter and total brain. Decreases in hippocampal and gray matter are typical markers of Alzheimer’s dementia-related neurodegeneration. MRIs also showed a greater volume of white matter hyperintensities, which are white spots on the brain that cause an area to decline in functionality.

Episodic memory and working memory were related to hippocampal volume, but perceptual speed was associated with white matter hyperintensities in the study, showing that results from the memory tests and the MRI were complementary.

“In the absence of effective treatments for dementia, we need to monitor and control cardiovascular risk burden as a way to maintain patient’s cognitive health as they age,” said Weili Xu, PhD, Department of Epidemiology and Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, China. “Given the progressive increase in the number of dementia cases worldwide, our findings have both clinical and public health relevance.”

Study limitations include that participants were volunteers from the community, which could limit the generalizability of the findings, and that participants were generally well-educated and performed relatively well on cognitive tests, so the observed association may have been an underestimation.

In a related editorial comment, Costantino Iadecola, MD, Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, said exploring the use of a common cardiovascular risk score like FGCRS to assess cognitive decline is highly relevant.

“The results of this study suggest a useful tool for assessing dementia risk and support recommendations to aggressively manage cardiovascular risk factors in midlife,” Iadecola said.

Source: The American College of Cardiology


Today’s Comic

Get Moving, Seniors: It’s Good For Your Brain

Want to give your brain a boost? Go for a swim, take a walk, or spin your partner on the living room floor.

A new study finds that aerobic exercise can improve older adults’ thinking and memory, even if they’re longtime couch potatoes.

This type of exercise increases blood flow to the brain and counters the effects of normal aging, according to the study published online May 13 in the journal Neurology.

“As we all find out eventually, we lose a bit mentally and physically as we age. But even if you start an exercise program later in life, the benefit to your brain may be immense,” said study author Marc Poulin, of the University of Calgary School of Medicine in Canada.

“Sure, aerobic exercise gets blood moving through your body. As our study found, it may also get blood moving to your brain, particularly in areas responsible for verbal fluency and executive functions. Our finding may be important, especially for older adults at risk for Alzheimer’s and other dementias and brain disease,” Poulin said in a journal news release.

The study included 206 adults, average age 66, with no history of memory or heart problems.

For six months, they took part in supervised exercise program three times a week. As they progressed, their workout increased from an average 20 minutes a day to least 40 minutes. They were also asked to work out on their own once a week.

At the end of the exercise program, participants had a 5.7% improvement on tests of executive function, which includes mental abilities used to focus, plan, recall instructions and multi-task. They also had 2.4% increase in verbal fluency, a measure of how quickly a person can retrieve information.

“This change in verbal fluency is what you’d expect to see in someone five years younger,” Poulin said.

On average, blood flow to their brain increased 2.8% — a gain tied to a number of improvements in types of thinking that typically decline with age.

“Our study showed that six months’ worth of vigorous exercise may pump blood to regions of the brain that specifically improve your verbal skills as well as memory and mental sharpness,” Poulin said.

“At a time when these results would be expected to be decreasing due to normal aging, to have these types of increases is exciting,” he said.

Source: HealthDay


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Tiny RNA that Should Attack Coronavirus Diminish with Age, Disease

Toni Baker wrote . . . . . . . . .

A group of tiny RNA that should attack the virus causing COVID-19 when it tries to infect the body are diminished with age and chronic health problems, a decrease that likely helps explain why older individuals and those with preexisting medical conditions are vulnerable populations, investigators report.

MicroRNAs play a big role in our body in controlling gene expression, and also are a front line when viruses invade, latching onto and cutting the RNA, the genetic material of the virus, says Dr. Sadanand Fulzele, aging researcher in the Department of Medicine and Center for Healthy Aging at the Medical College of Georgia at Augusta University.

But with age and some chronic medical conditions, the attacking microRNA numbers dwindle, reducing our ability to respond to viruses, says Dr. Carlos M. Isales, co-director of the MCG Center for Healthy Aging and chief of the MCG Division of Endocrinology, Diabetes and Metabolism.

Much like not having enough troops on the ground in an actual war, the coronavirus is then better able to do what it does naturally, which is hijack our cell machinery so it can replicate, say the researchers who report in the journal Aging and Disease what appear to be key microRNA involved in responding to this virus. They have a longer-term goal of identifying the biggest hitters and replenishing those troops.

They looked at the RNA sequence of actually two coronaviruses, SARS, which surfaced in 2002, and SARS-CoV-2, which causes COVID-19, and the sequence of the microRNAs that appeared to be attacking the virus, then used computer simulation to figure out which would logically fit together like puzzle pieces. Their perusal included four samples of SARS and 29 samples of SARS-CoV-2, taken between January and April 2020 from five continents covering 17 countries from the United States to Germany to Thailand.

They found 848 microRNAs that target the SARS genome and 873 microRNAs that target SARS-CoV-2 genome. They found 558 of the microRNAs fighting SARS also present in SARS-CoV-2, while 315 microRNAs were unique to SARS-CoV-2, and 290 were unique to SARS. MicroRNAs most proficient at attacking SARS-CoV-2 showed more than 10 target sites and might ultimately be found to be the most proficient at fighting the virus, which, in a few months, has changed much of the way the world functions.

They also found the microRNAs targeting SARS-CoV-2 were associated with more than 72 biological processes — from the production of molecules to the immune response — and that many are known to become dysregulated and/or diminish in number with age and with underlying medical conditions like diabetes and cardiovascular disease, a likely factor in the increased disease presentation and death rates seen in these individuals, the investigators say.

An example is microRNAs like miR-15b-5p, which has a high affinity for SARS-CoV-2, but is downregulated in coronary artery disease, says corresponding author Fulzele. In healthy, younger people, these microRNAs whose nature is to bind to the virus, are more apt to do as they should and prevent replication, he adds.

In the 29 worldwide samples of SARS-CoV-2, 19 had identical microRNAs, which indicates the virus has a fairly uniform presence internationally and that any effective treatments or vaccines should have broad impact, Isales says.

Next steps include studies in culture and lab animals to ensure findings are consistent with the computer analysis of human microRNAs in this study.

“The most important and striking feature of COVID-19 is the increased case fatality rate in aged individuals,” the investigators write, with the CDC reporting that nearly half of patients requiring hospitalization are age 65 and older, and these more senior individuals account for about 80% of the deaths. Fulzele, Isales and their colleagues wanted to know more about why.

“My perspective is there is a key set of microRNAs that are important in triggering this abnormal response, in making older patients more susceptible,” says senior author Isales. “We are looking at microRNAs in general dropping, but there is a specific subset that is key. The question is whether we can we target those as a therapy.”

Cocktails of multiple key microRNA, potentially given through the nose, might help restore sufficient levels of the key virus fighters, the investigators say.

They already are moving toward producing synthetic microRNA that could supplement this frontline weakened by age or disease, Fulzele says. Future studies also include pinning down which microRNA would be most impactful as an adjunct therapy, for example with the drug remdesivir, under study now for COVID-19, which works to stop the virus’ pirating of healthy cell machinery.

Another question to pursue is whether some younger people, who also are seriously sickened by SARS-CoV-2 infection, already don’t make sufficient numbers of some of the key protective microRNA, Isales says.

The microRNA present in the cells of our body typically target both the 3’-UTR (three prime untranslated region) region of the virus, the section of messenger RNA that contains regulatory regions that influence gene expression and protein function, as well as the coding region that ultimately produces a protein, unless they are outnumbered.

“Normally your immune cells would go in and destroy them but you have this large viral load as they continue to replicate and you have all this abrupt inflammatory response,” says Isales, which ultimately results in the cytokine storms that help destroy rather than protect organs. He thinks the reduced number of key microRNA critical to the body attacking the virus is an enabler of the disaster than can follow.

SARS and SARS-CoV-2 sequences used in the study were received from the National Center for Biotechnology Information and the GISAID, an international initiative to share data from the influenza viruses and the SARS-CoV-2 strain. The genome sequence of SARS and SARS-CoV-2 were retrieved from GenBank, the National Institutes of Health’s genetic sequence database. The scientists used the whole viral genome sequence for microRNA target analysis.

SARS, or severe acute respiratory syndrome, first surfaced in China and spread worldwide but while it was more deadly than the current coronavirus, it was not as infectious so less people ultimately died than are succumbing to COVID-19, Isales says. Worldwide, 8,098 people were infected with SARS and 774 died, according to the Centers for Disease Control and Prevention. Near the end of the first week in May, there were nearly 1.3 million SARS-CoV-2 cases confirmed in the United States alone and more than 76,000 deaths.

People age 65 and older and people of any age with underlying medical conditions, are considered at higher risk for severe illness from COVID-19, according to the Centers for Disease Control and Prevention. Underlying medical conditions include problems like serious heart conditions, chronic lung disease and moderate to severe asthma, and people with a compromised immune system such as individuals with cancer or who have had an organ transplant, the CDC says. Obesity, diabetes, chronic kidney disease requiring dialysis and liver disease are among the other conditions.

Source: Augusta University


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Study: Cognition and Gait Speed Often Decline Together

Will Sansom wrote . . . . . . . . .

Do thinking and walking go hand in hand in determining the health course of senior adults? A study published by UT Health San Antonio researchers found that, indeed, the two functions often parallel each other in determining a person’s health trajectory.

The researchers analyzed data from 370 participants in the San Antonio Longitudinal Study of Aging (SALSA) and found that they grouped into three distinct trajectories. These classifications were based on the participants’ changes on a cognitive measure and a gait speed task over an average of 9½ years:

  • Stable cognition and gait class (65.4% of the participants).
  • Cognitive and physical vulnerability class (22.2%).
  • Physical vulnerability class (12.4%).

“In our community-based sample of Mexican American and European American older adults aged 65 to 74 years old at baseline, the majority of individuals began the study with higher scores in both domains, cognition and gait speed. During follow-up, this group demonstrated resilience to age-related declines and continued to be functionally independent,” said study senior author Helen Hazuda, Ph.D., professor in UT Health San Antonio’s Long School of Medicine and the principal investigator of SALSA.

“In contrast, one-fifth of individuals began the study with lower scores in cognition and gait speed. They experienced deterioration in each domain during the follow-up period,” Dr. Hazuda said.

The third group of individuals, termed the physical vulnerability class, demonstrated stable cognition throughout the study, but their gait speed slowed over time.

2 effects, 1 root?

Cognition was assessed using English or Spanish versions of the Folstein Mini-Mental State Examination, a 30-item tool that assesses orientation to time and place, attention, recall, language and other aspects. Gait speed was measured with a timed 10-foot walk.

“For most of the population we studied, changes in cognition and gait speed were parallel, which suggests shared mechanisms,” said Mitzi M. Gonzales, Ph.D., lead author of the study and a neuropsychologist with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, which is part of UT Health San Antonio.

Cognition and gait speed may be altered by blood vessel disease, brain tissue insults, hormone regulation, and abnormal deposits of amyloid beta and tau proteins in the brain, Dr. Gonzales said. Amyloid beta and tau deposits are well-known indicators of Alzheimer’s disease but may impact gait, too.

“Abnormal protein deposition promotes neurodegeneration and synaptic loss, which may induce dysfunction in brain regions governing cognition and gait,” said study coauthor Sudha Seshadri, M.D., professor of neurology in the Long School of Medicine and director of the Biggs Institute. “Another possibility is damage to white matter in regions integral to both cognition and gait coordination.”

Groundbreaking San Antonio research

SALSA investigators led by Dr. Hazuda launched the study in 1992 and completed the baseline examination in 1996. Follow-up examinations were conducted at 18-month intervals between 2000 and 2005.

Among the 370 participants in this new analysis, 182 were Mexican American and 188 were European American. The Mexican American participants were almost four times more likely than European Americans to be in the cognitive and physical vulnerability class, even after statistical adjustment for educational attainment, income and chronic medical conditions, Dr. Gonzales said.

Prevalence of a key risk factor in this group, diabetes, was significantly higher in Mexican Americans (23%) than in European Americans (7%). Diabetes was associated with a 4½ times higher likelihood of being part of the cognitive and physical vulnerability class.

Poor start, poor course

Individuals who entered the study with poorer cognition and slower gait speed went on to decline in both domains at an accelerated pace through the years of follow-up, Dr. Hazuda said.

“In this at-risk group, we observed steeper rates of decline over and above the low starting point,” Dr. Hazuda said. “This suggests that preventive efforts should ideally target young and middle-aged adults in which there is still time to intervene to alter the trajectories.”

Overall, individuals in the cognitive and physical vulnerability class and the physical vulnerability class had a five- to sevenfold increased risk of mortality in comparison to the stable cognition and gait class.

The International Journal of Geriatric Psychiatry published the study in April.

Source: The University of Texas