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Over the last few decades, the mainstream theory of Alzheimer's disease (amyloid deposits build up in the brain) and medical treatments (drugs) just hasn't led anywhere. Nothing has worked to stop Alzheimer's disease. But evidence is building for an alternative view - that microbes in the brain are leading to the development of Alzheimer's disease (here and here). Now new compelling evidence from studies implicates several strains of herpes virus in Alzheimer's disease. At least one study has suggested herpes zoster, others the common herpes simplex, while other studies suggest other herpes strains. Which means that treatment could perhaps involve anti-viral drugs! (Wouldn't it be great if that works???)

In one study researchers found that human herpes virus DNA and RNA were more abundant in the brains of those diagnosed with Alzheimer's disease and that "abundance correlated with clinical dementia scores" - meaning the more of it, the sicker the person was. And the two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders.

The article mentions another recently published study from Taiwan. This amazing study looked at more than 33,000 individuals in Taiwan and found that patients with herpes simplex infections (HSV) may have a 2.56-fold increased risk of developing dementia. And they found that the use of anti-herpetic (antiviral) medications in the treatment of HSV infections was associated with a decreased risk of dementia - that the risk dropped back down "to baseline". The conclusion was that the antiviral medication reduced the risk of Alzheimer’s by keeping the herpes infection in check. Yes! Finally, a way foreward in this horrible disease.

Scroll down and read what one group of researchers says: "Our model right now is that it’s not just a single microbe, but a disturbance in the brain microbiome that can lead to Alzheimer’s disease.”

From A. Azvolinsky's article at The Scientist: Herpes Viruses Implicated in Alzheimer’s Disease

The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being amended to a newer one, which posits that microbes may trigger Alzheimer’s pathology ...continue reading "Herpes Viruses and Alzheimer’s Disease"

The last post dealt with the link between highly processed food and increased risk of cancer. Now an interesting article written by Dr. Lisa Mosconi (Associate Director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College/New York -Presbyterian Hospital) refers to that study when discussing research about lifestyles (and especially diet) and later Alzheimer's disease.

It'll be interesting to see how this research plays out - is her approach stressing diet (and avoiding ultra-processed food and trans fats) and lifestyle correct or not? Much of what she says definitely makes sense and is supported by research, such as the negative health effects of chronic inflammation, and how eating actual, real foods has beneficial health effects. On the other hand, vitamin, mineral, and fish oil supplements generally don't show those health benefits (as she discusses here).

Currently there are a number of theories about causes of Alzheimer's disease (including the role of microbes), as well as a number of drug treatments that so far have gone nowhere. If Dr. Mosconi's research interests you, then read the interview she did in 2017. [In the interview she talks about the importance of exercise, intellectual stimulation, social networks, and the benefits of eating real foods rather than supplements. She recommends: drink water, eat fish, eat vegetables and fruit, eat glucose rich foods, and don't eat highly processed and fast foods.]  From Quartz:

The road to Alzheimer’s disease is lined with processed foods

Dementia haunts the United States. There’s no one without a personal story about how dementia has touched someone they care for. But beyond personal stories, the broader narrative is staggering: By 2050, we are on track to have almost 15 million Alzheimer’s patients in the US alone. ... It’s an epidemic that’s already underway—but we don’t recognize it as such. The popular conception of Alzheimer’s is as an inevitable outcome of aging, bad genes, or both.  ...continue reading "Ultra-Processed Foods and Alzheimer’s?"

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.

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.

This post is more on the theme of nanoparticles and human health. My last post was about a study that examined how inhaled nanoparticles  (for example, from air pollution) travel from the lungs to the bloodstream. Well, today's post is about a pretty shocking 2016 air pollution nanoparticle study which examined the brains (brain tissue) of 45 dead people  (ages 3 to 92) who had lived for a long time in two places with heavy  particulate air pollution - Mexico City and Manchester, England. Some of the British people also had Alzheimer's disease or dementia.

The researchers found evidence that minute nano-sized particles of magnetite from air pollution can find their way into the brain. There are 2 forms of magnetite (which is an iron ore) - one naturally occurring (jagged edges in appearance), and one found commonly in air pollution (smooth and rounded - from being created in the high temperatures of vehicle engines or braking systems). The researchers are concerned that the air pollution nanoparticles may increase the risk for brain diseases such as Alzheimer's.

One of the researchers (Prof Barbara Maher) has previously identified magnetite particles in samples of air gathered beside a busy road in Lancaster, England and outside a power station. She suspected that similar particles may be found in the brain samples, and that is what happened. "It's dreadfully shocking. When you study the tissue you see the particles distributed between the cells and when you do a magnetic extraction there are millions of particles, millions in a single gram of brain tissue - that's a million opportunities to do damage."..."It's a whole new area to investigate to understand if these magnetite particles are causing or accelerating neurodegenerative disease." However, it must be stressed that at this time there is no proven link between these magnetite particles and any neurodegenerative diseases. They're just wondering.... they call finding these pollution nanoparticles "suggestive observations".

From Medical Xpress: Toxic air pollution nanoparticles discovered in the human brain

Tiny magnetic particles from air pollution have for the first time been discovered to be lodged in human brains – and researchers think they could be a possible cause of Alzheimer's disease. Researchers at Lancaster University found abundant magnetite nanoparticles in the brain tissue from 37 individuals aged three to 92-years-old who lived in Mexico City and Manchester. This strongly magnetic mineral is toxic and has been implicated in the production of reactive oxygen species (free radicals) in the human brain, which are associated with neurodegenerative diseases including Alzheimer's disease.

Professor Barbara Maher, from Lancaster Environment Centre, and colleagues (from Oxford, Glasgow, Manchester and Mexico City) used spectroscopic analysis to identify the particles as magnetite. Unlike angular magnetite particles that are believed to form naturally within the brain, most of the observed particles were spherical, with diameters up to 150 nm, some with fused surfaces, all characteristic of high-temperature formation – such as from vehicle (particularly diesel) engines or open fires. The spherical particles are often accompanied by nanoparticles containing other metals, such as platinum, nickel, and cobalt.

Professor Maher said: "The particles we found are strikingly similar to the magnetite nanospheres that are abundant in the airborne pollution found in urban settings, especially next to busy roads, and which are formed by combustion or frictional heating from vehicle engines or brakes."

Other sources of magnetite nanoparticles include open fires and poorly sealed stoves within homes. Particles smaller than 200 nm are small enough to enter the brain directly through the olfactory nerve after breathing air pollution through the nose.....The results have been published in the paper 'Magnetite pollution nanoparticles in the human brain' by the Proceedings of the National Academy of Sciences.

A good discussion of the study in The Scientist: Environmental Magnetite in the Human Brain

Image of magnetite nanoparticles from the exhaust plume of a diesel engine. Credit Maher et al study, 2016.

 

 

A microscopic image shows magnetite nanoparticles in the human brain. Barbara Maher et al study, 2016.

 

 

A study found that daily drinking of  tea (either black tea/oolong or green tea) is associated with a lower risk of "neurocognitive disorders" - in cognitive impairment in women, and in a lower risk of Alzheimer's disease in both men and women who are genetically predisposed to the disease (apolipoprotein E (APOE) genotype) - when compared to those who never or rarely drank tea. The researchers called long-term daily tea drinking as "neuroprotective".

The study followed 957 residents of Singapore for several years. All were "cognitively normal" when the study started (average age 64 1/2 years), but 72 people or 7.5% had developed neurocognitive disorders by the second follow-up (after 4 years). The study found that there was a dose-dependent relationship - the more tea that was drunk daily, the more protective it appeared to be. And it was most protective in those who consistently drank tea at both time points - when the study started and till the end. However, there was a gender difference - it seemed to protect women from neurocognitive disorders, but not men. But in those who were genetically predisposed to Alzheimer's - tea drinking was protective for both males and females. Further studies will follow up to see if the gender difference holds - they couldn't explain it.

The researchers also point out that tea drinking has a long history in Chinese culture as an natural "attention enhancer" and strong tea is drunk as to maintain alertness and concentration. Sounds a lot like why people drink coffee. From Medical Xpress:

Daily consumption of tea protects the elderly from cognitive decline

Tea drinking reduces the risk of cognitive impairment in older persons by 50 per cent and as much as 86 per cent for those who are genetically at risk of Alzheimer's. A cup of tea a day can keep dementia away, and this is especially so for those who are genetically predisposed to the debilitating disease, according to a recent study led by Assistant Professor Feng Lei from the Department of Psychological Medicine at National University of Singapore's (NUS) Yong Loo Lin School of Medicine. The longitudinal study involving 957 Chinese seniors aged 55 years or older has found that regular consumption of tea lowers the risk of cognitive decline in the elderly by 50 per cent, while APOE e4 gene carriers who are genetically at risk of developing Alzheimer's disease may experience a reduction in cognitive impairment risk by as much as 86 per cent.

He added, "Based on current knowledge, this long term benefit of tea consumption is due to the bioactive compounds in tea leaves, such as catechins, theaflavins, thearubigins and L-theanine. These compounds exhibit anti-inflammatory and antioxidant potential and other bioactive properties that may protect the brain from vascular damage and neurodegeneration. Our understanding of the detailed biological mechanisms is still very limited so we do need more research to find out definitive answers.

Remember all the dietary advice that for years told us to avoid or limit consumption of eggs - that since they were high in cholesterol, they were bad for us and would increase our risk for heart disease? And the nonsense that we should only eat the egg whites while throwing out the yolks? Hah...That advice was wrong, which another recent study confirms.

Eggs are an amazingly nutritious food. They’re loaded with high quality protein, healthy fats, vitamins, minerals, high in choline (a brain nutrient), biotin, antioxidants, lutein, and zeaxanthin. One review of studies (involving millions of people) looked at whole egg consumption  and found that high egg consumption (up to one egg per day) is not associated with increased risk of coronary heart disease or stroke, and in fact there was a reduced risk of hemorrhagic stroke. Only among diabetics was there an elevated risk of coronary heart disease with high egg consumption (up to 1 egg per day). Another study found a lower risk of type 2 diabetes in middle-aged men (see post).

A recent study from Finland found that neither cholesterol nor egg intake (eating one egg per day) was associated with an increased risk of dementia or Alzheimer's disease in Finnish men who were followed for 22 years. Instead, eating eggs was associated with better cognitive performance in certain areas such as executive function, which includes memory, problem solving, and planning (they were given neuropsychological tests). From Science Daily:

High cholesterol intake and eggs do not increase risk of memory disorders

A new study from the University of Eastern Finland shows that a relatively high intake of dietary cholesterol, or eating one egg every day, are not associated with an elevated risk of dementia or Alzheimer's disease. Furthermore, no association was found in persons carrying the APOE4 gene variant that affects cholesterol metabolism and increases the risk of memory disorders. APOE4 is common in Finland.

The dietary habits of 2,497 men aged between 42 and 60 years and with no baseline diagnosis of a memory disorder were assessed at the onset the Kuopio Ischaemic Heart Disease Risk Factor Study, KIHD, in 1984-1989 at the University of Eastern Finland. During a follow-up of 22 years, 337 men were diagnosed with a memory disorder, 266 of them with Alzheimer's disease. 32.5 per cent of the study participants were carriers of APOE4.

The study found that a high intake of dietary cholesterol was not associated with the risk of dementia or Alzheimer's disease -- not in the entire study population nor in the carriers of APOE4. Moreover, the consumption of eggs, which are a significant source of dietary cholesterol, was not associated with the risk of dementia or Alzheimer's disease. On the contrary, the consumption of eggs was associated with better results in certain tests measuring cognitive performance

Recently some studies have found that a diminished sense of smell occurs in persons with mild cognitive impairment and Alzheimer's disease. Doctors have long observed that patients with Alzheimer's frequently complain that food doesn't taste good anymore (because they can't smell what they are eating). This is because odor signals from the nose are processed in areas of the brain that are among the first to be affected by Alzheimer's disease. It is thought that as dementia starts and progresses, the parts of the brain that distinguish odors start to deteriorate.

This is why various odor tests have been devised. One such odor test (used in the following study) is called "Sniffin Sticks", which tests for 16 odors such as orange, peppermint, leather, banana, garlic, rose, fish, and coffee. However, note that other degenerative brain diseases (including Parkinson's) can also affect odor detection, and the ability to smell can be diminished by smoking, certain head injuries, and even normal aging. From Medical Xpress:

Study confirms 'sniff test' may be useful in diagnosing early Alzheimer's disease

Tests that measure the sense of smell may soon become common in neurologists' offices. Scientists have been finding increasing evidence that the sense of smell declines sharply in the early stages of Alzheimer's, and now a new study from the Perelman School of Medicine at the University of Pennsylvania published today in the Journal of Alzheimer's Disease confirms that administering a simple "sniff test" can enhance the accuracy of diagnosing this dreaded disease. The sniff test also appears to be useful for diagnosing a pre-dementia condition called mild cognitive impairment (MCI), which often progresses to Alzheimer's dementia within a few years.

Roalf and his colleagues used a simple, commercially available test known as the Sniffin' Sticks Odor Identification Test, in which subjects must try to identify 16 different odors. They administered the sniff test, and a standard cognitive test (the Montreal Cognitive Assessment), to 728 elderly people. The subjects had already been evaluated by doctors at Penn with an array of neurological methods, and according to expert consensus had been placed in one of three categories: "healthy older adult," "mild cognitive impairment," or "Alzheimer's dementia." Roalf and his team used the results from the cognitive test alone, or combined with the sniff test, to see how well they identified subjects in each category.

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

Prompted by prior studies that have linked a weakening sense of smell to Alzheimer's, doctors in a few larger dementia clinics already have begun to use smell tests in their assessments of elderly patients. Part of the reason the practice has not yet become common is that the tests that seem most useful take too long to administer. 

 Eating several servings of seafood (especially fish) weekly has beneficial health effects throughout life, and now research finds another benefit in older adults. Seafood contains both EPA and DHA, which are two types of omega-3 fatty acids. DHA or docosahexanoic acid has "neuroprotective qualities" and is found in both the gray and white matter of the brain. Higher DHA levels (measured in the blood) was associated with better memory, less brain atrophy (better brain volume), and fewer amyloid plaques (which are associated with Alzheimer's) in cognitively healthy older adults. From Medscape:

Higher Serum DHA Linked to Less Amyloid, Better Memory

New research supports neuroprotectant effects of docosahexaenoic acid (DHA) in the aging brain. In a small cross-sectional study of cognitively healthy older adults, higher serum DHA levels were associated with less cerebral amyloidosis, better memory scores, and less regional brain atrophy.

"The interesting finding was the association of low serum DHA levels with cerebral amyloidosis (amyloid plaques) in older adults without evidence of dementia," Hussein N. Yassine, MD, Department of Medicine, University of Southern California, Los Angeles, told Medscape Medical News. "This association was predominantly driven by persons at the lowest quartile of serum DHA levels who likely have limited intake of seafood." "This study adds to the existing evidence on the benefit of seafood consumption on [Alzheimer's disease] AD risk factors," Dr Yassine added.

The study was published online August 8 in JAMA Neurology. In a linked editorial, Joseph F. Quinn, MD, Department of Neurology, Oregon Health and Science University, Portland, notes that DHA is "the most abundant polyunsaturated fatty acid in the brain, playing an important structural role in synapses while also modulating a number of signaling pathways. "Brain DHA levels are also modulated by dietary intake, so it is plausible for dietary DHA to alter brain concentrations and affect downstream targets including brain pathology and function."

Dr Yassine and colleagues assessed serum DHA levels, measures of amyloid burden based on positron emission tomography with Pittsburgh compound B, brain volume, and neuropsychological test scores in 61 adults without dementia in the Aging Brain Study.

They found that serum DHA levels (percentage of total fatty acids) were 23% lower in those with cerebral amyloidosis relative to those without. Serum DHA levels were inversely correlated with brain amyloid load, independent of age, sex, years of education, and apolipoprotein E genotype. They also noted a positive correlation between serum DHA levels and brain volume in several subregions affected by AD, in particular the left subiculum and the left entorhinal volumes.

Clinically, there was a significant association between serum DHA levels and nonverbal memory. This association persisted after adjustment for age but not after adjustment for apolipoprotein E genotype. Serum DHA levels were not associated with measures of global cognition, executive function, or verbal memory scores.

Get out there and start getting active NOW - the earlier you start in life, the better for your brain decades later. All physical activity or exercise is good, including regular walks. From Medical Xpress:

Regular exercise protects against cognitive decline in later years

Regular exercise in middle age is the best lifestyle change a person can make to prevent cognitive decline in the later years, a landmark 20-year study has found.

University of Melbourne researchers followed 387 Australian women from the Women's Healthy Ageing Project for two decades. The women were aged 45 to 55-years-old when the study began in 1992. The research team made note of their lifestyle factors, including exercise and diet, education, marital and employment status, number of children, mood, physical activity and smoking....They were also asked to learn a list of 10 unrelated words and attempt to recall them half an hour later, known as an Episodic Verbal Memory test.

When measuring the amount of memory loss over 20 years, frequent physical activity, normal blood pressure and high good cholesterol were all strongly associated with better recall of the words. Study author Associate Professor Cassandra Szoeke, who leads the Women's Healthy Ageing Project, said once dementia occurs, it is irreversible. "In our study more weekly exercise was associated with better memory." 

"We now know that brain changes associated with dementia take 20 to 30 years to develop," Associate Professor Szoeke said. "The evolution of cognitive decline is slow and steady, so we needed to study people over a long time period. We used a verbal memory test because that's one of the first things to decline when you develop Alzheimer's Disease."
Regular exercise of any type, from walking the dog to mountain climbing, emerged as the number one protective factor against memory loss. Asoc Prof Szoeke said that the best effects came from cumulative exercise, that is, how much you do and how often over the course of your life.  (Original study)