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Interesting study results - being overweight (a higher body mass index or BMI) is linked to dementia more than 20 years later, but in the few years before dementia onset body mass index (BMI) is lower in those who develop dementia than in those who don't develop dementia. The researchers hypothesize that 2 processes are going on:  A higher BMI (overweight or obese) in mid-life is harmful (a direct effect), and then there is weight loss during the preclinical dementia phase. Bottom line: best is a normal weight in mid-life to try to prevent dementia later on in life. From Science Daily:

Obesity increases dementia risk

People who have a high body mass index (BMI) are more likely to develop dementia than those with a normal weight, according to a new UCL-led study. The study, published in the Alzheimer's & Dementia journal, analysed data from 1.3 million adults living in the United States and Europe. The researchers also found that people near dementia onset, who then go on to develop dementia, tend to have lower body weight than their dementia-free counterparts.

"The BMI-dementia association observed in longitudinal population studies, such as ours, is actually attributable to two processes," said lead author of the study, Professor Mika Kivimäki (UCL Institute of Epidemiology & Health). "One is an adverse effect of excess body fat on dementia risk. The other is weight loss due to pre-clinical dementia. For this reason, people who develop dementia may have a higher-than-average body mass index some 20 years before dementia onset, but close to overt dementia have a lower BMI than those who remain healthy."

In this study, researchers from across Europe pooled individual-level data from 39 longitudinal population studies from the United States, the United Kingdom, France, Sweden, and Finland. A total of 1,349,857 dementia-free adults participated in these studies and their weight and height were assessed. Dementia was ascertained using linkage to electronic health records obtained from hospitalisation, prescribed medication and death registries.

A total of 6,894 participants developed dementia during up to 38 years of follow-up. Two decades before symptomatic dementia, higher BMI predicted dementia occurrence: each 5-unit increase in BMI was associated with a 16-33% higher risk of this condition (5 BMI units is 14.5 kg for a person 5'7" (170 cm) tall, approximately the difference in weight between the overweight and normal weight categories or between the obese and overweight categories). In contrast, the mean level of BMI during pre-clinical stage close to dementia onset was lower compared to that in participants who remained healthy. [Original study.]

It's reassuring to see that there are positive things one can do to maintain brain health as one ages. With normal aging, the brain typically shrinks a little with each passing decade  - starting from about the age of 40. But one recent Australian study, which reviewed the results of many other studies, found that exercise slows down this shrinkage in humans, specifically in the left hippocampus. That is, that aerobic exercise had a significant positive effect on the volume of the left hippocampus. This matches the result of animal studies.

The researchers pointed out that some studies found increases also in other parts of the human brain from exercise (e.g. in the white matter), but that they did not look at and review those studies. [See posts on research.] The good news is that positive effects were from exercise programs generally lasting less than 12 months. But it is unknown which type of exercise is best, or whether it is general "activity level and movement" that is most important. Bottom line: Get out there and move, move, move for brain health. And for cardiorespiratory fitness. It's all linked and it's all good. From Medical Xpress:

Exercise maintains brain size, new research finds

Aerobic exercise can improve memory function and maintain brain health as we age, a new Australian-led study has found. In a first of its kind international collaboration, researchers from Australia's National Institute of Complementary Medicine at Western Sydney University and the Division of Psychology and Mental Health at the University of Manchester in the UK examined the effects of aerobic exercise on a region of the brain called the hippocampus, which is critical for memory and other brain functions.

Brain health decreases with age, with the average brain shrinking by approximately five per cent per decade after the age of 40. Studies in mice and rats have consistently shown that physical exercise increases the size of the hippocampus but until now evidence in humans has been inconsistent.

The researchers systematically reviewed 14 clinical trials which examined the brain scans of 737 people before and after aerobic exercise programs or in control conditions. The participants included a mix of healthy adults, people with mild cognitive impairment such as Alzheimer's and people with a clinical diagnosis of mental illness including depression and schizophrenia. Ages ranged from 24 to 76 years with an average age of 66. The researchers examined effects of aerobic exercise, including stationary cycling, walking, and treadmill running. The length of the interventions ranged from three to 24 months with a range of 2-5 sessions per week.

Overall, the results – published in the journal NeuroImage– showed that, while exercise had no effect on total hippocampal volume, it did significantly increase the size of the left region of the hippocampus in humans.

"When you exercise you produce a chemical called brain-derived neurotrophic factor (BDNF), which may help to prevent age-related decline by reducing the deterioration of the brain," Mr Firth said. "Our data showed that, rather than actually increasing the size of the hippocampus per se, the main 'brain benefits' are due to aerobic exercise slowing down the deterioration in brain size. In other words, exercise can be seen as a maintenance program for the brain.".... Interestingly, physical exercise is one of the very few 'proven' methods for maintaining brain size and functioning into older age.

I can't resist posting excerpts from a recent article announcing that researchers just found an entirely new lymph system ("lymphatic vessels") in the brain that transports fluid in the brain, and is probably "crucial to metabolic and inflammatory processes".  The image in this post shows the system in the brain. Amazing that it is only now "discovered" - apparently it was noticed by an anatomist 2 centuries ago, but this was pooh-poohed by modern day physicians. Until now. Excerpts from the Atlantic:

Scientists Somehow Just Discovered a New System of Vessels in Our Brains

You are now among the first people to see the brain’s lymphatic system. The vessels in the photo above transport fluid that is likely crucial to metabolic and inflammatory processes. Until now, no one knew for sure that they existed. Doctors practicing today have been taught that there are no lymphatic vessels inside the skull. Those deep-purple vessels were seen for the first time in images published this week by researchers at the U.S. National Institute of Neurological Disorders and Stroke.

In the rest of the body, the lymphatic system collects and drains the fluid that bathes our cells, in the process exporting their waste. It also serves as a conduit for immune cells, which go out into the body looking for adversaries and learning how to distinguish self from other, and then travel back to lymph nodes and organs through lymphatic vessels.

Senior investigator Daniel Reich trained as both a neurologist and radiologist, and his expertise is in inflammatory brain disease. The connection between the immune system and the brain is at the core of what he says he spends most of his time thinking about: multiple sclerosis. The immune system appears to modulate or even underlie many neurologic diseases, and the cells of the central nervous system produce waste that needs to be washed away just like other metabolically active cells. This discovery should make it possible to study how the brain does that, how it circulates white blood cells, and how these processes may go awry in diseases or play a role in aging.

Around the same time, researchers discovered fluid in the brains of mice and humans that would become known as the “glymphatic system.” It was described by a team at the University of Rochester in 2015 as not just the brain’s “waste-clearance system,” but as potentially helping fuel thebrain by transporting glucose, lipids, amino acids, and neurotransmitters.

Wouldn’t neurosurgeons, at some point in their meticulous down-to-the-millimeter dissecting of brains, have stopped and said, “Hey ... what’s this thing?”The lymph vessels probably escaped detection because they’re inside a thick membrane, the dura mater, which is the consistency of leather. They run alongside blood vessels that are much larger, and on MRI the signal that creates the images is dominated by the blood vessels.  

But this pathway appears crucial to life and health. A 2013 study in Science found that glymphatic flow seems to increase by almost double during sleep (in mice). Sleep disturbances are a common feature in Alzheimer’s and other neurologic disorders, and it’s possible that inadequate clearing of the brain’s waste products is related to exacerbating or even causing the disease.... 

The flow of glymphatic fluid can change based on a person’s intake of omega-3 fatty acids, a study showed earlier this year. Preliminary findings like these together suggest a pathway through which nutrition and sleep can be related to neurologic disorders. Optimizing this glymphatic flow could become a central theme for the future of neurologic health. “If all of this is true, there probably is a connection between these two systems, glymphatic and lymphatic,” Reich said. “And that would be one of the major functions of cerebrospinal fluid.”

From The Atlantic. Credit: Daniel Reich/ National Institute of Neurological Disorders and Stroke

For years studies have suggested that eating blueberries and other berries is good for our health (here, here, and here). Now another study suggests that eating wild blueberries benefits children's thinking, specifically attention and "executive function" (mental processes which lets people plan, organize, and complete tasks). What was nice in this study was that it was "double-blind"- which meant that biases couldn't influence the results. 

Flavonoids are a diverse group of phytonutrients (plant chemicals) found in almost all fruits and vegetables. They are powerful antioxidants with anti-inflammatory and immune system benefits. And yes, other studies have also found various benefits to mental processes with an increase of flavonoids in the diet - in both children and adults.

What foods contain flavonoids? There are 6 main classes of flavonoids, and each is found in different foods: - Anthocyanidins – found in red, purple,and blue berries, red wine, and red and purple grapes. - Flavonols - found in onions, leeks, broccoli, Brussels sprouts, kale, tea, berries, beans, and apples. - Flavones - found in parsley, celery, and hot peppers. - Isoflavones - found in soybeans, soy products, and legumes. - Flavanones - found in citrus fruit and tomatoes. - Flavanols - found in tea, red wine, grapes, apples, fava beans, and cocoa. From Medical Xpress:

Primary school children could show better attention by consuming flavonoid-rich blueberries, following a study conducted by the University of Reading. In a paper published in Food & Function, a group of 7-10 year olds who consumed a drink containing wild blueberries or a matched placebo and were tested on their speed and accuracy in completing an executive task function on a computer.The double blind trial found that the children who consumed the flavonoid-rich blueberry drink had 9% quicker reaction times on the test without any sacrifice of accuracy. In particular, the effect was more noticeable as the tests got harder.

Previous [Univ. of] Reading research has shown that consuming wild blueberries can improve mood in children and young people, simple memory recall in primary school children, and that other flavonoid rich drinks such as orange juice, can also improve memory and concentration.

Wild blueberries are grown and harvested in North America, and are smaller than regular blueberries, and are higher in flavonoids compared to regular varieties. The double-blind trial used a flavonoid-rich wild blueberry drink, with a matched placebo contained 8.9 g of fructose, 7.99 g of glucose and 4 mg of vitamin C matching the levels of nutrients found in the blueberry drink. [Original study.] 

Interesting study finding - that both high and low levels of magnesium is associated with a higher risk of dementia. Magnesium is an essential mineral needed for more than 300 biochemical reactions in the body. According to a large study done in the Netherlands of people who were followed for about 8 years - there was a U-shaped incidence of dementia based on their levels of magnesium. The lowest incidence was in those with "in the middle" normal levels of magnesium in the blood. All the study participants were mentally healthy when the study started.

The researchers stated that magnesium levels are considered "relatively stable over time", but a limitation of the study is that they only looked at magnesium levels once - at the beginning of the study, so they could have changed over time. Of course further studies are needed. [Other posts on magnesium and health - here, here, and here.]

Magnesium is widely available in foods. Foods that are good sources of magnesium include: spinach and other dark green leafy vegetables, almonds, cashews, peanuts, bananas, soybeans, kidney and black beans (legumes), whole grains, lentils, seeds, yogurt, brown rice, potatoes, and avocados. It is recommended that magnesium is obtained from the diet, and not from supplements (due to health risks from high doses). From Science Daily:

Both high, low levels of magnesium in blood linked to risk of dementia

People with both high and low levels of magnesium in their blood may have a greater risk of developing dementia, according to a study published in the September 20, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology.

The study involved 9,569 people with an average age of 65 who did not have dementia whose blood was tested for magnesium levels. The participants were followed for an average of eight years. During that time, 823 people were diagnosed with dementia. Of those, 662 people had Alzheimer's disease. The participants were divided into five groups based on their magnesium levels. Both those with the highest and the lowest levels of magnesium had an increased risk of dementia, compared to those in the middle group.

Both the low and high groups were about 30 percent more likely to develop dementia than those in the middle group. Of the 1,771 people in the low magnesium group, 160 people developed dementia, which is a rate of 10.2 per 1,000 person-years. For the high magnesium group, 179 of the 1,748 people developed dementia, for a rate of 11.4 per 1,000 person-years. For the middle group, 102 of the 1,387 people developed dementia, for a rate of 7.8. Kieboom noted that almost all of the participants had magnesium levels in the normal range, with only 108 people with levels below normal and two people with levels above normal[Original study.]

Another article was published this month raising the issue of whether Alzheimer's disease is caused by a microbe - which can explain why all the medicines and experimental drugs aimed at treating the "tangles" or amyloid plaques in the brain are not working as a treatment (because that's the wrong approach). The microbe theory of Alzheimer's disease has been around for decades, but only recently is it starting to be taken seriously. Some of the microbes found in patients with Alzheimer's disease (from analyses of both normal brains and Alzheimer patient brains after death): fungi, Borrelia burgdorferi (Lyme disease), herpes simplex virus Type 1 (HSV1), and Chlamydia pneumoniae.

The general hypotheses seem to be that Alzheimer’s disease is caused by infection, but it isn't linked to any one pathogenic microbe.  Instead, the evidence seems to support that "following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation". So the microbes act as "triggers" for Alzheimer's disease - the microbes get into the brain, and immune responses somehow eventually result in the amyloid plaques and Alzheimer's disease. From The Scientist:

Do Microbes Trigger Alzheimer’s Disease?

In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease. Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.

Allen had recently proposed a novel role for biofilms—colonies of bacteria that adhere to surfaces and are largely resistant to immune attack or antibiotics—in eczema....  Allen knew of recent work showing that Lyme spirochetes form biofilms, which led him to wonder if biofilms might also play a role in Alzheimer’s disease. When Allen stained for biofilms in brains from deceased Alzheimer’s patients, he found them in the same hippocampal locations as amyloid plaquesToll-like receptor 2 (TLR2), a key player in innate immunity, was also present in the same region of the Alzheimer’s brains but not in the controls. He hypothesizes that TLR2 is activated by the presence of bacteria, but is locked out by the biofilm and damages the surrounding tissue instead.

Spirochetes, common members of the oral microbiome, belong to a small set of microbes that cross the blood-brain barrier when they’re circulating in the blood, as they are during active Lyme infections or after oral surgery. However, the bacteria are so slow to divide that it can take decades to grow a biofilm. This time line is consistent with Alzheimer’s being a disease of old age, Allen reasons, and is corroborated by syphilis cases in which the neuroinvasive effects of spirochetes might appear as long as 50 years after primary infection.

Allen’s work contributes to the revival of a long-standing hypothesis concerning the development of Alzheimer’s. For 30 years, a handful of researchers have been pursuing the idea that pathogenic microbes may serve as triggers for the disease’s neuropathology..... In light of continued failures to develop effective drugs, some researchers, such as Harvard neurobiologist Rudolph Tanzi, think it’s high time that more effort and funding go into alternative theories of the disease. “Any hypothesis about Alzheimer’s disease must include amyloid plaques, tangles, inflammation—and, I believe, infection.”

Herpes simplex virus type 1 (HSV1) can acutely infect the brain and cause a rare but very serious encephalitis. In the late 1980s, University of Manchester molecular virologist Ruth Itzhaki noticed that the areas of the brain affected in HSV1 patients were the same as those damaged in patients with Alzheimer’s disease. Knowing that herpes can lie latent in the body for long periods of time, she began to wonder if there was a causal connection between the infection and the neurodegenerative disorder.

Around the same time, neuropathologist Miklossy, then at the University of Lausanne in Switzerland, was detailing the brain damage caused by spirochetes—both in neurosyphilis and neuroborrelia, a syndrome caused by Lyme bacteria. She happened upon a head trauma case with evidence of bacterial invasion and plaque formation, and turned her attention to Alzheimer’s. She isolated spirochetes from brain tissue in 14 Alzheimer’s patients but detected none in 13 age-matched controls. In addition, monoclonal antibodies that target the amyloid precursor protein (APP)—which, when cleaved, forms amyloid-β—cross-reacted with the spirochete species found, suggesting the bacteria might be the source of the protein.

Meanwhile, in the U.S., a third line of evidence linking Alzheimer’s to microbial infection began to emerge. While serving on a fraud investigation committee, Alan Hudson, a microbiologist then at MCP-Hahnemann School of Medicine in Philadelphia, met Brian Balin.... Soon, Balin began to send Hudson Alzheimer’s brain tissue to test for intracellular bacteria in the Chlamydia genus. Some samples tested positive for C. pneumoniae: specifically, the bacteria resided in microglia and astrocytes in regions of the brain associated with Alzheimer’s neuropathology, such as the hippocampus and other limbic system areas. Hudson had a second technician repeat the tests before he called Balin to unblind the samples. The negatives were from control brains; the positives all had advanced Alzheimer’s disease. "We were floored,” Hudson says.

Thus, as early as the 1990s, three laboratories in different countries, each studying different organisms, had each implicated human pathogens in the etiology of Alzheimer’s disease. But the suggestion that Alzheimer’s might have some microbial infection component was still well outside of the theoretical mainstream. Last year, Itzhaki, Miklossy, Hudson, and Balin, along with 29 other scientists, published a review in the Journal of Alzheimer’s Disease to lay out the evidence implicating a causal role for microbes in the disease.

The microbe theorists freely admit that their proposed microbial triggers are not the only cause of Alzheimer’s disease. In Itzhaki’s case, some 40 percent of cases are not explained by HSV1 infection. Of course, the idea that Alzheimer’s might be linked to infection isn’t limited to any one pathogen; the hypothesis is simply that, following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation.

Two studies looked at manganese and found that high levels are associated with problems. Manganese is an essential trace mineral necessary for development, metabolism, the antioxidant system, and for normal brain and nerve function. Getting manganese through foods (e.g. nuts, seeds, whole grains) is beneficial, but ingesting large amounts through supplements or being exposed to high levels in some other way (such as polluted air) is associated with various health problems. 

The first study found that high manganese in the diet (in mice) was associated with an increased risk of staph (Staphylococcus aureus) heart infection. The second study (done in East Liverpool, Ohio) found that exposure to consistently high levels of manganese in the air is associated with lower IQ scores in children. And why did the air the children were breathing have high levels of manganese? Because there was a nearby hazardous waste incinerator and a facility that handles manganese.

From Medical Xpress: Excess dietary manganese promotes staph heart infection

Too much dietary manganese—an essential trace mineral found in leafy green vegetables, fruits and nuts—promotes infection of the heart by the bacterium Staphylococcus aureus ("staph"). The findings, reported this week in the journal Cell Host & Microbe, add to the evidence that diet modifies risk for infection. The discovery also suggests that people who have excess levels of tissue manganese, including those who consume dietary supplements with high concentrations of the metal, may be at increased risk for staph infection of the heart.

Skaar and his colleagues studied the impact of dietary manganese on staph infection in a mouse model. Most of the mice that consumed a high manganese diet—about three times more manganese than normal—died after infection with staph. The investigators discovered that the animals on the high manganese diet were particularly susceptible to staph infection of the heart, which was a surprise, said Skaar, who is also professor of Pathology, Microbiology and Immunology.... The researchers found that excess manganese inactivates a key line of defense against pathogens: the innate immune system's reactive oxygen burst. 

Staph is the leading cause of bacterial endocarditis (infection of the inner lining of the heart chamber and heart valves) and the second most frequent cause of bloodstream infections. Interestingly, some populations of people have both increased risk for staph infections, particularly endocarditis, and higher than normal levels of tissue manganese, Skaar noted. These populations include intravenous drug users, patients with chronic liver disease and patients on long-term intravenous diets.

From Medical Xpress: Higher manganese levels in children correlate with lower IQ scores, study finds

A study led by environmental health researchers at the University of Cincinnati (UC) College of Medicine finds that children in East Liverpool, Ohio with higher levels of Manganese (Mn) had lower IQ scoresThe study analyzed blood and hair samples of 106 children 7 to 9 years of age from East Liverpool and surrounding communities, who enrolled in the study from March 2013 to June 2014.... The study found that increased Mn in hair samples was significantly associated with declines in full-scale IQ, processing speed and working memory.

Manganese is an element generally found in combination with iron and many minerals. It plays a vital role in brain growth and development, but excessive exposure can result in neurotoxicity. Manganese is used widely in the production of steel, alloys, batteries and fertilizers and is added to unleaded gasolineLocated in northeast Ohio along the Ohio River, East Liverpool has a demonstrated history of environmental exposures, with EPA records showing elevated levels of manganese concentrations since 2000.... all  [air] monitors in East Liverpool had "consistently exceeded" health-based guidelines set by the agency.

 Manganese (Mn). Credit: Wikipedia

Surprised...is how I felt after reading this study. According to the study, activity levels and exercise in mid-life are not linked to cognitive fitness and dementia later on in life. Instead, higher levels of physical activity and exercise has a beneficial effect on the brain in the short term (e.g., within 2 years or so). This finding of no long-term benefits, but only short-term benefits to the brain from exercise, is contrary to some other (cross-sectional) studies, but is supported by another recent study ("no evidence of a neuroprotective effect of physical activity").

The beauty of this study is that it followed 646 people for 30 years (from a median age of 46 years in 1978 and 77 years in 2008). The negative is that according to this study, physical exercise in mid-life does not seem to delay or prevent the onset of dementia and Alzheimer's later on in life. Eh... From Medical Xpress:

Physical activity in midlife not linked to cognitive fitness in later years, long-term study shows

A study led by Johns Hopkins Bloomberg School of Public Health researchers that tracked activity levels of 646 adults over 30 years found that, contrary to previous research, exercise in mid-life was not linked to cognitive fitness in later yearsThe finding suggests that physical activity may not help maintain cognitive function, or help avoid or delay the onset of the debilitating conditions like dementia and Alzheimer's

The study, which appears online in the Journal of Alzheimer's Disease, did find that activity levels among study participants in the later years were associated with high cognitive function two years later. This supports earlier research findings that exercise may help to maintain cognitive fitness in the short term.

There is no known treatment or cure for Alzheimer's or dementia, syndromes that involves declining memory, confusion and eventually limited ability to perform daily tasks. To date, there are no preventive measures, such as physical exercise, brain games or a diet regimen, that have been proven to help delay or altogether prevent its onset. The researchers undertook the study because of a growing consensus that physical activity levels helps prevent Alzheimer's, however much of the evidence for this thinking is based on cross-sectional studies that compare responses from one group of participants with another at a given point in time or within a very short duration, typically several years..... That's where longitudinal studies, which look at the same group of participants over a long time, are more helpful.

The researchers used data from the Johns Hopkins Precursors study.... The researchers used responses from 1978 through 2008 from 646 participants (598 men, 48 women) to calculate so-called metabolic equivalents, which quantify physical activity levels. Participants were also asked whether they regularly exercise to a sweat. The team administered cognitive tests in 2008, and, using participants' medical records, scored for dementia through 2011. The researchers identified 28, or 4.5 percent of the cohort, to have Alzheimer's.

No physical activity measure in mid-life was associated with late-life cognitive fitness or onset of dementia. The study confirmed findings of other cross-sectional studies, that higher levels of physical activity and exercise measured close in time to the cognitive testing were associated with better cognitive functioning. The authors also looked at whether patterns of change in physical activity levels over the life span were associated with cognitive health and found no relationships.

The idea that exercise might play a role in preventing or limiting Alzheimer's makes sense, the researchers say, because physical activity, at least in mouse models, has shown less accumulation of B-amyloid plaques, which are thought to play a role in dementia, including Alzheimer's. In addition, physical activity improves blood flow to the brain, which is linked to better cognitive performance. This may explain why studies find that exercise may contribute to cognitive fitness in the short term.

  Should tackle football continue to be played in its current form? A study with horrifying results that was published this week in the Journal of the American Medical Association raises that question once again. The study examined 202 brains of people who had formerly played football for varying lengths of time and at varying levels (some who only played pre-high school, some at high school, college level, semi-professional, or Canadian football league). They found the highest percentage of  the degenerative brain disease chronic traumatic encephalopathy (CTE) among former NFL players (110 out of 111 brains). However, the overall incidence of CTE was 87% when looking at all 202 brains. They also found that the 3 out of 14 former high school players had mild CTE, but the majority of former college, semiprofessional, and professional players had severe CTE.

The one thing to keep in mind is that the study only examined donated brains of former football players  - which means that the family members were concerned about CTE in the former player (perhaps there were symptoms suggestive of CTE). So we don't know the actual percentage of CTE in currently playing and former football players. But studies (here. here, and here) do show damage from hits received during football games and practice at even the grammar and high school level - and the damage can be from subconcussive hits.

But note that concussions and subconcussive hits (head trauma) also occur in other sports, such as soccer. Everyone agrees we need more studies, and we also need to rethink how some games are played in childhood to protect developing brains. From NPR:

Study: CTE Found In Nearly All Donated NFL Player Brains

As the country starts to get back into its most popular professional team sport, there is a reminder of how dangerous football can be. An updated study published Tuesday by the Journal of the American Medical Association on football players and the degenerative brain disease chronic traumatic encephalopathy reveals a striking result among NFL players. The study examined the brains of deceased former football players (CTE can only be diagnosed after death) and found that 110 out of 111 brains of those who played in the NFL had CTE. CTE has been linked to repeated blows to the head — the 2015 movie Concussion chronicled the discovery of CTE's connection to football.

In the study, researchers examined the brains of 202 deceased former football players at all levels. Nearly 88 percent of all the brains, 177, had CTE. Three of 14 who had played only in high school had CTE, 48 of 53 college players, 9 of 14 semiprofessional players, and 7 of 8 Canadian Football League players. CTE was not found in the brains of two who played football before high school.

CTE study several years ago by McKee and her colleagues included football players and athletes from other collision sports such as hockey, soccer and rugby. It also examined the brains of military veterans who had suffered head injuries. The study released Tuesday is the continuation of a study that began eight years ago. In 2015, McKee and fellow researchers at the Department of Veterans Affairs and Boston University published study results revealing 87 of 91 former NFL players had CTE.

McKee is chief of neuropathology at VA Boston Healthcare System and director of the CTE Center at the BU School of Medicine. Speaking about the new numbers, she says it's "startling to be able to gather 177 examples of CTE" in a relatively short period of time (the past eight years). "While we still don't know what the incidence is in the general population or in the general population of football players," she says, "the fact that we were able to gather this many cases [in that time frame] says this disease is much more common than we previously realized." "We need a very well-constructed longitudinal study," says McKee, "looking at young individuals playing these sports. We need to follow them for decades...." [Original study.]

  Lately more and more research has been finding health benefits with frequent consumption of extra virgin olive oil (EVOO). It is also a basic part of the popular Mediterranean diet - which emphasizes fresh fruits and vegetables, nuts, legumes (beans), whole grains, some fish, and extra virgin olive oil. Now a study conducted by investigators at Temple University in Philadelphia, Pennsylvania, suggests that the olive oil in the Mediterranean diet probably promotes healthy brain aging. The researchers said: "Our study is the first demonstration that EVOO can beneficially affect memory, amyloid plaques, and tau pathology, the hallmark lesions in the brain of Alzheimer's patients."

But... note that they are taking findings from their study done on mice and hypothesizing that this is what is also going on in humans.  Their study used specially bred mice (and only 22 in total) - one group which received extra virgin olive oil in their food (starting at 6 months of age), and the other not. The researchers found that after a few months of this diet that there were differences between the 2 groups when tested at 12 months (which is also when they were euthanized). Note that mice are short lived and after 6 months they are considered "mature adults".

The researchgers now plan to test varying daily doses of EVOO on humans soon - this way they can see what the minimal dosage is for beneficial effects (if any), and if there is a maximal dosage where there are negative health effects. In the meantime, enjoy olive oil in your diet - looks like it will benefit your health in a number of ways (herehere, and here). From Medscape:

Olive Oil Key Ingredient in Alzheimer's Prevention?

Extra-virgin olive oil (EVOO) appears to protect memory and learning ability and reduces the formation of beta amyloid (Aβ) plaques and neurofibrillary tangles in the brain — the classic hallmarks of Alzheimer's disease (AD) — new animal research shows. The study, conducted by investigators at Temple University in Philadelphia, Pennsylvania, suggests that it is the olive oil component of the Mediterranean diet that likely promotes healthy brain aging.... "And results are important enough to absolutely encourage people to consume greater amounts of EVOO. Given that it's been consumed for at least 2000 years, I do not anticipate any side effects," he added.

For the study, the investigators tested the potentially beneficial effects of EVOO on triple transgenic mice. These mice are specifically bred to develop key pathologic features of AD (Alzheimer's disese), including amyloid plaques and neurofibrillary tangles. The animals were divided into two groups. One group received EVOO-enriched chow, and the other received regular chow without EVOO. The olive oil was introduced into the diet when the mice were 6 months of age, before they began to develop symptoms of AD..... The mice were subjected to the same behavioral tests at both 9 and 12 months of age, after which they were euthanized and their brains were examined for the presence of key pathologic features of AD.

The researchers confirmed that mice fed the EVOO-enriched diet performed significantly better at both 9 and 12 months on tests designed to assess working memory, spatial memory, and learning abilities compared with mice fed regular chow. The researchers also found a statistically significant reduction in the amount of Aβ peptides deposited in the brains of the EVOO-treated animals compared with controls. There was also a significant reduction in the phosphorylated forms of tau in mice fed the EVOO-enriched chow compared to controls, although olive oil had no effect on total tau levels in the same region of the brain.

The investigators also examined whether the improvements in cognitive performance and brain pathology that were observed in EVOO-treated mice might be the result of an improvement in synaptic integrity. Once again, they found greater preservation in the integrity of the synapses between neurons in EVOO-fed mice compared with controls....  Furthermore, there was a dramatic increase in nerve cell autophagy activation in brain cells from the EVOO-fed animals compared with controls. Dr Pratico explained that autophagy is a mechanism by which cells digest proteins that are produced in excess or that are abnormal. In this particular animal model, autophagy digests and gets rid of both amyloid plaques and phosphorylated tau.

"Thanks to the autophagy activation, memory and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer's disease were significantly reduced. This is a very important discovery, since we suspect that a reduction in autophagy marks the beginning of Alzheimer's disease."