Music on the brain

A neurological study of classical musicians trained in different styles

July 20, 2020

Science Daily/University of Tokyo

A new study looks at differences between the brains of Japanese classical musicians, Western classical musicians and nonmusicians. Researchers investigated specific kinds of neural behavior in participants as they were exposed to unfamiliar rhythms and nonrhythmic patterns. Trained musicians showed greater powers of rhythmic prediction compared to nonmusicians, with more subtle differences between those trained in Japanese or Western classical music. This research has implications for studies of cultural impact on learning and brain development.

"Music is ubiquitous and indispensable in our daily lives. Music can reward us, comfort us and satisfy us emotionally," said Project Assistant Professor Tatsuya Daikoku from the International Research Center for Neurointelligence at the University of Tokyo. "So it's no surprise the effect of music on the brain is well-researched. However, many studies focus on Western classical music, pop, jazz, etc., whereas ours is the first study that investigates neural mechanisms in practitioners of Japanese classical music, known as gagaku."

Many Japanese performance arts, such as in Noh or Kabuki theater, include music that does not necessarily follow a regular beat pattern as Western classical music typically does. That is, Japanese classical music sometimes expands or contracts beats without mathematical regularity. This time interval is often referred to as ma, which is an important notion throughout Japanese culture.

Daikoku and his research partner, Assistant Professor Masato Yumoto from the Graduate School of Medicine, explored how different groups of trained musicians and nonmusicians responded to different rhythm patterns. The idea was to see how musical training might influence statistical learning, the way our brains interpret and anticipate sequential information: in this case, rhythms.

The researchers recorded participants' brain activity directly using a technique called magnetoencephalography, which looks at magnetic signals in the brain. From the data, Daikoku and Yumoto were able to ascertain that statistical learning of the rhythms took place in the left hemisphere of participants' brains. And importantly, there was a greater level of activity in those with musical training, be it in Japanese or Western classical music.

"We expected that musicians would exhibit strong statistical learning of unfamiliar rhythm sequences compared to nonmusicians. This has been observed in previous studies which looked at responses to unfamiliar melodies. So this in itself was not such a surprise," said Daikoku. "What is really interesting, however, is that we were able to pick out differences in the neural responses between those trained in Japanese or Western classical music."

These differences between Japanese and Western classical musicians are far more subtle and become apparent in the higher-order neural processing of complexity in rhythm. Though it is not the case that one culture or another performed better or worse than the other, this finding does imply that different cultural upbringings and systems of education can have a tangible effect on brain development.

"This research forms part of a larger puzzle we wish to explore -- that of differences and similarities between the languages and music of cultures and how they affect learning and development," said Daikoku. "We also look into music as a way to treat developmental disorders such as language impairment. Personally, I hope to see a rejuvenation of interest in Japanese classical music; perhaps this study will inspire those unfamiliar with such music to hear and cherish this key part of Japanese cultural history."

https://www.sciencedaily.com/releases/2020/07/200720093255.htm

Biggest risk factors identified to try and prevent Alzheimer's disease

Clinicians should identify and target 10 risk factors in their attempt to prevent Alzheimer's disease, say researchers

July 20, 2020

Science Daily/BMJ

There are at least 10 risk factors that appear to have a significant impact on a person's likelihood of developing Alzheimer's disease that could be targeted with preventative steps, suggests research published in the Journal of Neurology, Neurosurgery & Psychiatry.

Focusing on these factors, which include cognitive activity, high body mass index in late life, depression, diabetes, and high blood pressure, could provide clinicians with an evidence based guideline for prevention of Alzheimer's disease, but a lot more research is needed to come up with other promising approaches to preventing the condition.

Currently, around 850,000 people in the UK are affected by dementia -- around two thirds of which are Alzheimer's disease -- and the condition is a leading cause of death, not helped by the fact that there have been no new drug treatments for dementia in almost 20 years.

Experts are predicting rising case numbers as the population ages but recent research has suggested that the number of cases appears to be reducing, possibly due to lifestyle changes, better education and risk reduction strategies to prevent or delay dementia.

Existing evidence on preventing Alzheimer's disease is challenging to interpret due to varying study designs with different endpoints and credibility.

So an international team of researchers led by Professor Jin-Tai Yu at Fudan University in China, set out to review and analyse current evidence in order to produce evidence-based suggestions on Alzheimer's disease prevention.

The researchers gathered 395 studies (243 observational prospective studies and 152 randomised controlled trials) that were suitable for their analysis.

From analysing these, they proposed 21 suggestions based on the consolidated evidence available that could be used in practice by clinicians to try to prevent Alzheimer's disease.

Within these, there were what they referred to as "Class I" suggestions to target 19 different factors.

Nearly two-thirds of these suggestions would involve targeting vascular risk factors (such as high blood pressure and cholesterol levels) and lifestyle, strengthening the importance of keeping healthy to prevent Alzheimer's disease.

Ten of the suggestions were backed by strong evidence and included receiving as much education as possible in early life, participating in mentally stimulating activities such as reading, avoiding diabetes, stress, depression, head trauma, and high blood pressure in midlife.

A further nine suggestions had slightly weaker evidence to support them and included regular physical exercise, getting sufficient good quality sleep, maintaining a healthy body weight and good heart health in later life, avoiding smoking, and including vitamin C in the diet.

In contrast, two interventions were not recommended -- oestrogen replacement therapy and use of acetylcholinesterase inhibitors (drugs that increase communication between nerve cells).

The authors point to some study limitations, such as the fact that observational studies cannot indicate a clear causal relationship and randomised controlled trials cannot be generalisable beyond the specific sample, intervention, dose and duration studied.

In addition, the values of their suggestions might be limited by geographic variability, definition of exposure and prevalence of risk factors at population level.

Nevertheless, the authors say this was the most comprehensive and large-scale systematic review and meta-analysis for Alzheimer's disease to date, and the evidence based suggestions were put together by integrating a large amount of evidence from different types of existing research.

They conclude: "This study provides an advanced and contemporary survey of the evidence, suggesting that more high-quality observational prospective studies and randomised controlled trials are urgently needed to strengthen the evidence base for uncovering more promising approaches to preventing Alzheimer's disease."

https://www.sciencedaily.com/releases/2020/07/200720190920.htm

'Love hormone' oxytocin could be used to treat cognitive disorders like Alzheimer's

July 20, 2020

Science Daily/Tokyo University of Science

Alzheimer's disease progressively degrades a person's memory and cognitive abilities, often resulting in dementia. Amid efforts to find novel treatments for this disease, a recent breakthrough study by scientists from Japan shows that oxytocin―the hormone that we commonly know to induce feelings of love and well-being―can also effectively reverse some of the damage caused by amyloid plaques in the learning and memory center of the brain in an animal model of Alzheimer's.

Alzheimer's disease is a progressive disorder in which the nerve cells (neurons) in a person's brain and the connections among them degenerate slowly, causing severe memory loss, intellectual deficiencies, and deterioration in motor skills and communication. One of the main causes of Alzheimer's is the accumulation of a protein called amyloid β (Aβ) in clusters around neurons in the brain, which hampers their activity and triggers their degeneration. Studies in animal models have found that increasing the aggregation of Aβ in the hippocampus―the brain's main learning and memory center―causes a decline in the signal transmission potential of the neurons therein. This degeneration affects a specific trait of the neurons, called "synaptic plasticity," which is the ability of synapses (the site of signal exchange between neurons) to adapt to an increase or decrease in signaling activity over time. Synaptic plasticity is crucial to the development of learning and cognitive functions in the hippocampus. Thus, Aβ and its role in causing cognitive memory and deficits have been the focus of most research aimed at finding treatments for Alzheimer's.

Now, advancing this research effort, a team of scientists from Japan, led by Professor Akiyoshi Saitoh from the Tokyo University of Science, has looked at oxytocin, a hormone conventionally known for its role in the female reproductive system and in inducing the feelings of love and well-being. "Oxytocin was recently found to be involved in regulating learning and memory performance, but so far, no previous study deals with the effect of oxytocin on Aβ-induced cognitive impairment," Prof Saitoh says. Realizing this, Prof Saitoh's group set out to connect the dots.

Prof Saitoh and team first perfused slices of the mouse hippocampus with Aβ to confirm that Aβ causes the signaling abilities of neurons in the slices to decline or―in other words―impairs their synaptic plasticity. Upon additional perfusion with oxytocin, however, the signaling abilities increased, suggesting that oxytocin can reverse the impairment of synaptic plasticity that Aβ causes.

To find out how oxytocin achieves this, they conducted a further series of experiments. In a normal brain, oxytocin acts by binding with special structures in the membranes of brain cells, called oxytocin receptors. The scientists artificially "blocked" these receptors in the mouse hippocampus slices to see if oxytocin could reverse Aβ―induced impairment of synaptic plasticity without binding to these receptors. Expectedly, when the receptors were blocked, oxytocin could not reverse the effect of Aβ, which shows that these receptors are essential for oxytocin to act.

Oxytocin is known to facilitate certain cellular chemical activities that are important in strengthening neuronal signaling potential and formation of memories, such as influx of calcium ions. Previous studies have suspected that Aβ suppresses some of these chemical activities. When the scientists artificially blocked these chemical activities, they found that addition of oxytocin addition to the hippocampal slices did not reverse the damage to synaptic plasticity caused by Aβ. Additionally, they found that oxytocin itself does not have any effect on synaptic plasticity in the hippocampus, but it is somehow able to reverse the ill―effects of Aβ.

Prof Saitoh remarks, "This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus." This is only a first step and further research remains to be conducted in vivo in animal models and then humans before sufficient knowledge can be gathered to reposition oxytocin into a drug for Alzheimer's. But, Prof Saitoh remains hopeful. He concludes, "At present, there are no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired. Our study puts forth the interesting possibility that oxytocin could be a novel therapeutic modality for the treatment of memory loss associated with cognitive disorders such as Alzheimer's disease. We expect that our findings will open up a new pathway to the creation of new drugs for the treatment of dementia caused by Alzheimer's disease."

https://www.sciencedaily.com/releases/2020/07/200720093308.htm

Synapse-saving proteins discovered, opening possibilities in Alzheimer's, schizophrenia

July 17, 2020

Science Daily/University of Texas Health Science Center at San Antonio

Researchers at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) have discovered a new class of proteins that protect synapses from being destroyed. Synapses are the structures where electrical impulses pass from one neuron to another.

The discovery, published July 13 in the journal Nature Neuroscience, has implications for Alzheimer's disease and schizophrenia. If proven, increasing the number of these protective proteins could be a novel therapy for the management of those diseases, researchers said.

In Alzheimer's disease, loss of synapses leads to memory problems and other clinical symptoms. In schizophrenia, synapse losses during development predispose an individual to the disorder.

"We are studying an immune system pathway in the brain that is responsible for eliminating excess synapses; this is called the complement system," said Gek-Ming Sia, PhD, assistant professor of pharmacology in UT Health San Antonio's Long School of Medicine and senior author of the research.

"Complement system proteins are deposited onto synapses," Dr. Sia explained. "They act as signals that invite immune cells called macrophages to come and eat excess synapses during development. We discovered proteins that inhibit this function and essentially act as 'don't eat me' signals to protect synapses from elimination."

The system sometimes goes awry

During development, synapses are overproduced. Humans have the most synapses at the ages of 12 to 16, and from then to about age 20, there is net synapse elimination that is a normal part of the brain's maturation. This process requires the complement system.

In adults, synapse numbers are stable, as synapse elimination and formation balance out. But in certain neurological diseases, the brain somehow is injured and begins to overproduce complement proteins, which leads to excessive synapse loss.

"This occurs most notably in Alzheimer's disease," Dr. Sia said.

In mouse models of Alzheimer's disease, researchers have found that the removal of complement proteins from the brain protects it from neurodegeneration, he said.

"We've known about the complement proteins, but there was no data to show that there were actually any complement inhibitors in the brain," Dr. Sia said. "We discovered for the first time that there are, that they affect complement activation in the brain, and that they protect synapses against complement activation."

Future directions

Dr. Sia and his colleagues will seek to answer interesting questions, including:

• Whether complement system biology can explain why some people are more resistant and more resilient against certain psychiatric disorders;

• How the number of complement inhibitors can be changed and whether that could have clinical ramifications;

• Whether different neurons produce different complement inhibitors, each protecting a certain subset of synapses.

Regarding the last question, Dr. Sia said:

"This could explain why, in certain diseases, there is preferential loss of certain synapses. It could also explain why some people are more susceptible to synapse loss because they have lower levels of certain complement inhibitors."

The researchers focused on a neuronal complement inhibitor called SRPX2. The studies are being conducted in mice that lack the SRPX2 gene, that demonstrate complement system overactivation and that exhibit excessive synapse loss.

https://www.sciencedaily.com/releases/2020/07/200717133234.htm

Alzheimer's risk factors may be measurable in adolescents and young adults

July 30, 2020

Science Daily/Alzheimer's Association

Risk factors for Alzheimer's dementia may be apparent as early as our teens and 20s, according to new research reported at the Alzheimer's Association International Conference® (AAIC®) 2020.

These risk factors, many of which are disproportionately apparent in African Americans, include heart health factors -- such as high blood pressure, high cholesterol and diabetes -- and social factors like education quality. According to the Alzheimer's Association Alzheimer's Disease Facts and Figures report, older African Americans are about twice as likely to have Alzheimer's or other dementias as older whites.

"By identifying, verifying, and acting to counter those Alzheimer's risk factors that we can change, we may reduce new cases and eventually the total number of people with Alzheimer's and other dementia," said Maria C. Carrillo, Ph.D., Alzheimer's Association chief science officer. "Research like this is important in addressing health inequities and providing resources that could make a positive impact on a person's life."

"These new reports from AAIC 2020 show that it's never too early, or too late, to take action to protect your memory and thinking abilities," Carrillo said.

The Alzheimer's Association is leading the U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (U.S. POINTER), a two-year clinical trial to evaluate whether lifestyle interventions that simultaneously target many risk factors protect cognitive function in older adults who are at increased risk for cognitive decline. U.S. POINTER is the first such study to be conducted in a large, diverse group of Americans across the United States.

African American Youth At Higher Risk of Dementia

In a population of more than 714 African Americans in the Study of Healthy Aging in African Americans (STAR), Kristen George, Ph.D., MPH, of the University of California, Davis, and colleagues found that high blood pressure and diabetes, or a combination of multiple heart health-related factors, are common in adolescence and are associated with worse late-life cognition. Study participants were adolescents (n=165; ages 12-20), young adults (n=439; ages 21-34) and adults (n=110; ages 35-56). Mean age at cognitive assessment was 68.

Cognition was measured using in-person tests of memory and executive function. The researchers found that, in this study population, having diabetes, high blood pressure, or two or more heart health risk factors in adolescence, young adulthood, or mid-life was associated with statistically significantly worse late-life cognition. These differences persisted after accounting for age, gender, years since risk factors were measured, and education.

Before this report, little was known about whether cardiovascular disease (CVD) risk factors developed prior to mid-life were associated with late-life cognition. This is an important question because African Americans have a higher risk of CVD risk factors compared to other racial/ethnic groups from adolescence through adulthood.

According to the researchers, these findings suggest that CVD risk factors as early as adolescence influence late-life brain health in African Americans. Efforts to promote heart and brain healthy lifestyles must not only include middle-aged adults, but also younger adults and adolescents who may be especially susceptible to the negative impact of poor vascular health on the brain.

Early Adult BMI Associated With Late Life Dementia Risk

In what the authors say is the first study to report on the issue, higher early adulthood (age 20-49) body mass index (BMI) was associated with higher late-life dementia risk.

Relatively little is known about the role of early life BMI on the risk of Alzheimer and other dementias. The scientists studied a total of 5,104 older adults from two studies, including 2,909 from the Cardiovascular Health Study (CHS) and 2,195 from the Health, Aging and Body Composition study (Health ABC). Of the total sample, 18% were Black and 56% were women. Using pooled data from four established cohorts spanning the adult life course, including the two cohorts under the study, the scientists estimated BMI beginning at age 20 for all older adults of CHS and Health ABC.

For women, dementia risk increased with higher early adulthood BMI. Compared to women with normal BMI in early adulthood, dementia risk was 1.8 times higher among those who were overweight, and 2.5 times higher among those who were obese. Analyses were adjusted for midlife and late life BMI.

They found no association between midlife BMI and dementia risk among women.

For men, dementia risk was 2.5 times higher among those who were obese in early adulthood, 1.5 times higher among those who were overweight in mid-life and 2.0 times higher among those who were obese in mid-life, in models also adjusted for late life BMI.

For both women and men, dementia risk decreased with higher late life BMI.

Adina Zeki Al Hazzouri, Ph.D. of Columbia University and colleagues found that high BMI in adulthood is a risk factor for dementia in late life. The researchers suggest that efforts aimed at reducing dementia risk may need to begin earlier in life with a focus on obesity prevention and treatment.

Quality of Early-Life Education Influences Dementia Risk

In a diverse group of more than 2,400 people followed up to 21 years, higher quality early-life education was associated with better language and memory performance, and lower risk of late-life dementia. Results were somewhat different between men and women, and between Blacks and Whites in the study.

The study included 2,446 Black and White men and women, age 65 and older, enrolled in the Washington Heights/Inwood Columbia Aging Project who attended elementary school in the United States. A school quality variable based on historical measures included: mandatory school enrollment age, minimum dropout age, school term length, student-teacher ratio, and student attendance.

People who attended school in states with lower quality education had more rapid decline in memory and language as an older adult. Black women and men and White women who attended schools in states with higher quality education were less likely to develop dementia. According to the scientists, the results were explained, in part, because people who attend higher quality schools end up getting more years of school.

Justina Avila-Rieger, PhD, a postdoctoral research scientist at Columbia University Irving Medical Center and colleagues say the findings provide evidence that later life dementia risk and cognitive function is influenced by early-life state educational policies.

https://www.sciencedaily.com/releases/2020/07/200730092616.htm

Apathy not depression helps to predict dementia

July 13, 2020

Science Daily/University of Cambridge

Apathy offers an important early warning sign of dementia in individuals with cerebrovascular disease, but depression does not, new research led by the University of Cambridge suggests.

Depression is often thought to be a risk factor for dementia but this may be because some depression scales used by clinicians and researchers partially assess apathy, say scientists from the universities of Cambridge, King's College London, Radboud and Oxford.

The study, published on 11 July in the Journal of Neurology, Neurosurgery & Psychiatry is the first to examine the relationships between apathy, depression, and dementia in individuals with cerebral small vessel disease (SVD). SVD may occur in one out of three elderly individuals, causes about a quarter of all strokes, and is the most common cause of vascular dementia.

The team studied two independent cohorts of SVD patients, one from the UK and the other from the Netherlands.* Across both cohorts, they found that individuals with higher baseline apathy, as well as those with increasing apathy over time, had a greater risk of dementia. In contrast, neither baseline depression nor change in depression had any detectable influence on dementia risk.

These findings were consistent despite variation in the severity of participants' symptoms, suggesting that they could be generalised across a broad spectrum of SVD cases. The relationship between apathy and dementia remained after controlling for other well-established risk factors for dementia including age, education, and cognition.

Lead author, Jonathan Tay, from Cambridge's Department of Clinical Neurosciences said: "There has been a lot of conflicting research on the association between late-life depression and dementia. Our study suggests that may partially be due to common clinical depression scales not distinguishing between depression and apathy."

Apathy, defined as a reduction in 'goal-directed behaviour', is a common neuropsychiatric symptom in SVD, and is distinct from depression, which is another symptom in SVD. Although there is some symptomatic overlap between the two, previous MRI research linked apathy, but not depression, with white matter network damage in SVD.

Jonathan Tay said: "Continued monitoring of apathy may be used to assess changes in dementia risk and inform diagnosis. Individuals identified as having high apathy, or increasing apathy over time, could be sent for more detailed clinical examinations, or be recommended for treatment."

Over 450 participants -- all with MRI-confirmed SVD -- recruited from three hospitals in South London and Radboud University's Neurology Department in the Netherlands, were assessed for apathy, depression and dementia over several years.

In the UK cohort, nearly 20% of participants developed dementia, while 11% in the Netherlands cohort did, likely due to the more severe burden of SVD in the UK cohort. In both datasets, patients who later developed dementia showed higher apathy, but similar levels of depression at baseline, compared to patients who did not.

The study provides the basis for further research, including the mechanisms that link apathy, vascular cognitive impairment, and dementia. Recent MRI work suggests that similar white matter networks underlie motivation and cognitive function in SVD. Cerebrovascular disease, which can be caused by hypertension and diabetes, can lead to network damage, resulting in an early form of dementia, presenting with apathy and cognitive deficits. Over time, SVD-related pathology increases, which is paralleled by increasing cognitive and motivational impairment, eventually becoming severe enough to meet criteria for a dementia state.

Jonathan Tay says: "This implies that apathy is not a risk factor for dementia per se, but rather an early symptom of white matter network damage. Understanding these relationships better could have major implications for the diagnosis and treatment of patients in the future."

https://www.sciencedaily.com/releases/2020/07/200713120022.htm

Exposure to air pollution impairs cellular energy metabolism

June 15, 2020

Science Daily/University of Eastern Finland

Exposure to air particulate matter impairs the metabolism of olfactory mucosal cells, according to a recent study from the University of Eastern Finland. The results can contribute to a better understanding of how air pollutants may harm brain health, as the olfactory mucosa can act as a key pathway to the brain.

In the last decade, the adverse effects of ambient air pollutants, including particulate matter, on the central nervous system is increasingly reported by epidemiological, animal and post-mortem studies. Exposure to air pollutants has been associated with neurodegenerative disorders, among other things. The association of air pollutant exposure with deteriorating brain health is speculated to be driven by particulate matter entry via the olfactory mucosa, a neural tissue located at the upper part of the nasal cavity. The olfactory mucosa consists of a mixture of diverse cell types that are important for the sense of smell, as the only neural tissue outside of the brain. It acts as a first line of defence against inhaled agents, including air pollutants. How air pollutant exposure affects this key brain entry site remains elusive.

The original research article published in Particle and Fibre Toxicology by the research group of Associate Professor Katja Kanninen from the University of Eastern Finland, sheds light on how exposure to particulate matter impacts the function of the human olfactory mucosa. The study was carried out with a new cellular model based on primary human olfactory mucosal cells.

Using sophisticated functional measurements and transcriptomic analyses, the researchers found that particulate matter exposure causes critical impairment in the metabolism of olfactory mucosal cells. These functions of mitochondria, the cellular organelles responsible for energy production, are disturbed by air pollutants. The researchers also identified the mitochondria-targeted NPTX1 gene, which has been shown previously to be associated with brain disorders, as a key driver of mitochondrial dysfunction upon particulate matter exposure.

According to Associate Professor Kanninen, the research carried out at the University of Eastern Finland may provide important insight into the effects of harmful environmental agents on the brain.

"Given the importance of the nasal cavity as a potential gateway to the brain by particles and external invaders, I believe that more studies should focus on discovering how exposure to environmental agents and factors affects the olfactory mucosa. This may one day lead to new ways of limiting the adverse health effects of airborne particle exposure," Associate Professor Kanninen notes.

https://www.sciencedaily.com/releases/2020/06/200615100929.htm

Study ties stroke-related brain blood vessel abnormality to gut bacteria

June 4, 2020

Science Daily/NIH/National Institute of Neurological Disorders and Stroke

In a nationwide study, NIH funded researchers found that the presence of abnormal bundles of brittle blood vessels in the brain or spinal cord, called cavernous angiomas (CA), are linked to the composition of a person's gut bacteria. Also known as cerebral cavernous malformations, these lesions which contain slow moving or stagnant blood, can often cause hemorrhagic strokes, seizures, or headaches. Current treatment involves surgical removal of lesions when it is safe to do so. Previous studies in mice and a small number of patients suggested a link between CA and gut bacteria. This study is the first to examine the role the gut microbiome may play in a larger population of CA patients.

Led by scientists at the University of Chicago, the researchers used advanced genomic analysis techniques to compare stool samples from 122 people who had at least one CA as seen on brain scans, with those from age- and sex-matched, control non-CA participants, including samples collected through the American Gut Project. Initially, they found that on average the CA patients had more gram-negative bacteria whereas the controls had more gram-positive bacteria, and that the relative abundance of three gut bacterial species distinguished CA patients from controls regardless of a person's sex, geographic location, or genetic predisposition to the disease. Moreover, gut bacteria from the CA patients appeared to produce more lipopolysaccharide molecules which have been shown to drive CA formation in mice. According to the authors, these results provided the first demonstration in humans of a "permissive microbiome" associated with the formation of neurovascular lesions in the brain.

Further analysis showed that some gut bacteria compositions could identify aggressive versus non-aggressive forms of the disease as well as those with recent symptomatic hemorrhages. Also, for the first time, they showed how combining gut bacteria data with results from blood plasma tests might help doctors better diagnose the severity of a brain disorder. The results, published in Nature Communications, support a growing body of evidence for the role of gut bacteria in brain health.

https://www.sciencedaily.com/releases/2020/06/200604095640.htm

Exercise improves memory, boosts blood flow to brain

Study: 1-year workout program shows benefits for older people at risk of dementia

May 20, 2020

Science Daily/UT Southwestern Medical Center

Scientists have collected plenty of evidence linking exercise to brain health, with some research suggesting fitness may even improve memory. But what happens during exercise to trigger these benefits? New UT Southwestern research that mapped brain changes after one year of aerobic workouts has uncovered a potentially critical process: Exercise boosts blood flow into two key regions of the brain associated with memory. Notably, the study showed this blood flow can help even older people with memory issues improve cognition, a finding that scientists say could guide future Alzheimer's disease research.

"Perhaps we can one day develop a drug or procedure that safely targets blood flow into these brain regions," says Binu Thomas, Ph.D., a UT Southwestern senior research scientist in neuroimaging. "But we're just getting started with exploring the right combination of strategies to help prevent or delay symptoms of Alzheimer's disease. There's much more to understand about the brain and aging."

Blood flow and memory

The study, published in the Journal of Alzheimer's Disease, documented changes in long-term memory and cerebral blood flow in 30 participants, each of them 60 or older with memory problems. Half of them underwent 12 months of aerobic exercise training; the rest did only stretching.

The exercise group showed 47 percent improvement in memory scores after one year compared with minimal change in the stretch participants. Brain imaging of the exercise group, taken while they were at rest at the beginning and end of the study, showed increased blood flow into the anterior cingulate cortex and the hippocampus -- neural regions that play important roles in memory function.

Other studies have documented benefits for cognitively normal adults on an exercise program, including previous research from Thomas that showed aging athletes have better blood flow into the cortex than sedentary older adults. But the new research is significant because it plots improvement over a longer period in adults at high risk to develop Alzheimer's disease.

"We've shown that even when your memory starts to fade, you can still do something about it by adding aerobic exercise to your lifestyle," Thomas says.

Mounting evidence

The search for dementia interventions is becoming increasingly pressing: More than 5 million Americans have Alzheimer's disease, and the number is expected to triple by 2050.

Recent research has helped scientists gain a greater understanding of the molecular genesis of the disease, including a 2018 discovery from UT Southwestern's Peter O'Donnell Jr. Brain Institute that is guiding efforts to detect the condition before symptoms arise. Yet the billions of dollars spent on researching how to prevent or slow dementia have yielded no proven treatments that would make an early diagnosis actionable for patients.

UT Southwestern scientists are among many teams across the world trying to determine if exercise may be the first such intervention. Evidence is mounting that it could at least play a small role in delaying or reducing the risk of Alzheimer's disease.

For example, a 2018 study showed that people with lower fitness levels experienced faster deterioration of vital nerve fibers in the brain called white matter. A study published last year showed exercise correlated with slower deterioration of the hippocampus.

Regarding the importance of blood flow, Thomas says it may someday be used in combination with other strategies to preserve brain function in people with mild cognitive impairment.

"Cerebral blood flow is a part of the puzzle, and we need to continue piecing it together," Thomas says. "But we've seen enough data to know that starting a fitness program can have lifelong benefits for our brains as well as our hearts."

https://www.sciencedaily.com/releases/2020/05/200520084123.htm

Early-life education improves memory in old age -- Especially for women

June 5, 2020

Science Daily/Georgetown University Medical Center

Education appears to protect older adults, especially women, against memory loss, according to a study by investigators at Georgetown University Medical Center, published in the journal Aging, Neuropsychology, and Cognition.

The results suggest that children -- especially girls -- who attend school for longer will have better memory abilities in old age. This may have implications for memory loss in Alzheimer's disease and other dementias.

The study tested declarative memory in 704 older adults (58-98 years of age). Declarative memory refers to our ability to remember events, facts, and words, such as where you put your keys or the name of that new neighbor.

Participants were shown drawings of objects, and then were tested several minutes later on their memory of these objects. The investigators found that their memory performance became progressively worse with aging. However, more years of early-life education countered these losses, especially in women.

In men, the memory gains associated with each year of education were two times larger than the losses experienced during each year of aging. However, in women, the gains were five times larger.

For example, the declarative memory abilities of an 80-year-old woman with a bachelor's degree would be as good as those of a 60-year-old woman with a high school education. So, four extra years of education make up for the memory losses from 20 years of aging.

"Simply said, learning begets learning" says the study's senior investigator, Michael Ullman, PhD, a professor in Georgetown's Department of Neuroscience and Director of the Brain and Language Lab. Ullman's research on the relationship between language, memory and the brain has been a cornerstone in the fields of language and cognitive neuroscience.

"Since learning new information in declarative memory is easier if it is related to knowledge we already have, more knowledge from more education should result in better memory abilities, even years later," adds the study's lead author, Jana Reifegerste, PhD, a member of the scientific staff at the University of Potsdam, Germany, who worked on this study as a postdoctoral researcher in Ullman's lab.

"Evidence suggests that girls often have better declarative memory than boys, so education may lead to greater knowledge gains in girls," says Ullman. "Education may thus particularly benefit memory abilities in women, even years later in old age."

The study tested individuals in a non-Western (Taiwanese) population. Participants varied in the number of years of education, from none at all to graduate studies. Future research is needed to test whether the findings generalize to other populations, Ullman says.

"These findings may be important, especially considering the rapidly aging population globally," Reifegerste says. "The results argue for further efforts to increase access to education."

"Education has also been found to delay the onset of Alzheimer's disease," Ullman says. "We believe that our findings may shed light on why this occurs."

https://www.sciencedaily.com/releases/2020/06/200605003035.htm