Tag Archives: Alzheimer’s disease (AD)

  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."

 Another study finding a link between air pollution and negative health effects - this time a higher incidence of decline in cognitive functioning  and dementia in older women (65 and older) exposed to fine particles (PM2.5 ). These extremely small particles from vehicle emissions are a major source of urban air pollution throughout the world. These results match other studies finding a link with urban air pollution, especially vehicle traffic, to negative effects on the brain (dementia, cognitive decline, shrinking of the brain, etc.). The researchers also exposed mice to this air pollution for 15 weeks and then studied their brains for evidence of degenerative effects in their brains - and yes, they did find them.

The researchers found that the adverse effects of fine particulate air pollution was stronger in both women and mice who had the APOE4 gene, a genetic variation that increases the risk for Alzheimer's disease. They said that while the air pollution has negative effects in general, that having the APOE4 gene interacted with the air pollution. The researchers also wrote that the mice studies they did showed that "...exposure to urban airborne particulates can intensify amyloid accumulation and neurodegeneration". Medical Xpress:

Air pollution may lead to dementia in older women

Tiny air pollution particles—the type that mainly comes from power plants and automobiles—may greatly increase the chance of dementia, including Alzheimer's disease, according to USC-led research. Scientists and engineers found that older women who live in places with fine particulate matter exceeding the U.S. Environmental Protection Agency's standard are 81 percent more at risk for global cognitive decline and 92 percent more likely to develop dementia, including Alzheimer's.

If their findings hold up in the general population, air pollution could be responsible for about 21 percent of dementia cases, according to the study. "Microscopic particles generated by fossil fuels get into our body directly through the nose into the brain," said University Professor Caleb Finch at the USC Leonard Davis School of Gerontology and co-senior author of the study. "Cells in the brain treat these particles as invaders and react with inflammatory responses, which over the course of time, appear to exacerbate and promote Alzheimer's disease.

The adverse effects were stronger in women who had the APOE4 gene, a genetic variation that increases the risk for Alzheimer's. "Our study .....provides the inaugural scientific evidence of a critical Alzheimer's risk gene possibly interacting with air particles to accelerate brain aging," said Jiu-Chiuan Chen, co-senior author of the study....[Their study] adds to an emerging body of research from around the world that links air pollution to dementia. The offending pollutants—known as PM2.5—are fine, inhalable particles with diameters 2.5 micrometers or smaller. A human hair is about 70 micrometers in diameter, making it 30 times larger than the largest PM2.5. The researchers analyzed data of 3,647 65- to 79-year-old women from the Women's Health Initiative Memory Study (WHIMS). These women lived across 48 states and did not have dementia when they enrolled.

USC scientists chronically exposed female mice carrying the APOE4 gene to nano-sized air pollution for 15 weeks. Compared to the control group, mice predisposed to Alzheimer's disease accumulated as much as 60 percent more amyloid plaque, the toxic clusters of protein fragments that further the progression of Alzheimer's.

In other studies, Chen and his colleagues linked long-term exposure to high PM2.5 levels to smaller gray and white matter volumes in important areas such as the frontal lobe, which carries out thinking, decision-making and planning. For every 3.5 micrograms of PM2.5 per cubic meter of air, white matter (insulated nerve fibers that connect different brain regions) decreased by 6 cubic centimeters, according to one earlier study. [see post]

 Interesting preliminary research that suggests that daily intake for 12 weeks of several beneficial bacteria species (Lactobacillus acidophilus, L. casei, L. fermentum, and Bifidobacterium bifidum) resulted in improved mental (cognitive) functioning in 52 people with Alzheimer's Disease. Could this be true - daily probiotics to improve mental functioning in those with Alzheimer's?

Many more studies need to be done, but this is definitely interesting. The nice thing in this study was that the patients were randomly assigned to the groups, and it was "double-blind" so no one knew who got just plain milk and who drank probiotic milk in the study (so no biases to distort results). There were also metabolic and inflammation improvements in those taking the probiotics. From Medical Xpress:

Probiotics improve cognition in Alzheimer's patients

For the first time, scientists have shown that probiotics—beneficial live bacteria and yeasts taken as dietary supplements—can improve cognitive function in humans. In a new clinical trial, scientists show that a daily dose of probiotic Lactobacillus and Bifidobacterium bacteria taken over a period of just 12 weeks is enough to yield a moderate but significant improvement in the score of elderly Alzheimer's patients on the Mini-Mental State Examination (MMSE) scale, a standard measure of cognitive impairment.

Probiotics are known to give partial protection against certain infectious diarrheas, irritable bowel syndrome, inflammatory bowel disease, eczema, allergies, colds, tooth decay, and periodontal disease. But scientists have long hypothesized that probiotics might also boost cognition, as there is continuous two-way communication between the intestinal microflora, the gastrointestinal tract, and the brain through the nervous system, the immune system, and hormones (along the so-called "microbiota-gut-brain axis"). In mice, probiotics have indeed been shown to improve learning and memory, and reduce anxiety and depression- and OCD-like symptoms. But prior to the present study there was very limited evidence of any cognitive benefits in humans.

Here, the researchers, from Kashan University of Medical Sciences, Kashan, and Islamic Azad University, Tehran, Iran, present results from a randomized, double-blind, controlled clinical trial on a total of 52 women and men with Alzheimer's between 60 and 95 years of age. Half of the patients daily received 200 ml milk enriched with four probiotic bacteria Lactobacillus acidophilus, L. casei, L. fermentum, and Bifidobacterium bifidum (approximately 400 billion bacteria per species), while the other half received untreated milk.

At the beginning and the end of the 12-week experimental period, the scientists took blood samples for biochemical analyses and tested the cognitive function of the subjects with the MMSE questionnaire, which includes tasks like giving the current date, counting backwards from 100 by sevens, naming objects, repeating a phrase, and copying a picture.

Over the course of the study, the average score on the MMSE questionnaire significantly increased (from 8.7 to 10.6, out of a maximum of 30) in the group receiving probiotics, but not in the control group (from 8.5 to 8.0). Even though this increase is moderate, and all patients remained severely cognitively impaired, these results are important because they are the first to show that probiotics can improve human cognition. Future research, on more patients and over longer time-scales, is necessary to test if the beneficial effects of probiotics become stronger after longer treatment.

Treatment with probiotics also resulted in lower levels of triglycerides, Very Low Density Lipoprotein (VLDL), high-sensitivity C-Reactive Protein (hs-CRP) in the blood of the Alzheimer patients, and likewise a reduction in two common measures (called "Homeostatic Model Assessment", HOMA-IR and HOMA-B) of insulin resistance and the activity of the insulin-producing cells in the pancreas. "These findings indicate that change in the metabolic adjustments might be a mechanism by which probiotics affect Alzheimer's and possibly other neurological disorders," says Salami. "We plan to look at these mechanisms in greater detail in our next study." [The original study.]

  Again, another study showing the importance of lifestyle factors in the development of protein buildups in the brain that are associated with the onset of Alzheimer's disease. Specifically, the study found that each one of several lifestyle factors—a healthy body mass index, physical activity and a Mediterranean diet, were linked to lower levels of plaques and tangles on brain scans in people who already had mild memory changes, (but not dementia). Other posts discussing Mediterranean diet and brain health (brain volume, etc.) are here, here, and here. Activity levels and brain health posts are here, here, and here. From Medical Xpress:

Diet and exercise can reduce protein build-ups linked to Alzheimer's

A study by researchers at UCLA's Semel Institute for Neuroscience and Human Behavior has found that a healthy diet, regular physical activity and a normal body mass index can reduce the incidence of protein build-ups that are associated with the onset of Alzheimer's disease.

In the study, 44 adults ranging in age from 40 to 85 (mean age: 62.6) with mild memory changes but no dementia underwent an experimental type of PET scan to measure the level of plaque and tangles in the brain. Researchers also collected information on participants' body mass index, levels of physical activity, diet and other lifestyle factors. Plaque, deposits of a toxic protein called beta-amyloid in the spaces between nerve cells in the brain; and tangles, knotted threads of the tau protein found within brain cells, are considered the key indicators of Alzheimer's.

The study found that each one of several lifestyle factors—a healthy body mass index, physical activity and a Mediterranean diet—were linked to lower levels of plaques and tangles on the brain scans. (The Mediterranean diet is rich in fruits, vegetables, legumes, cereals and fish and low in meat and dairy, and characterized by a high ratio of monounsaturated to saturated fats, and mild to moderate alcohol consumption.)

"The fact that we could detect this influence of lifestyle at a molecular level before the beginning of serious memory problems surprised us," said Dr. David Merrill, the lead author of the study, which appears in the September issue of the American Journal of Geriatric Psychiatry.

Earlier studies have linked a healthy lifestyle to delays in the onset of Alzheimer's. However, the new study is the first to demonstrate how lifestyle factors directly influence abnormal proteins in people with subtle memory loss who have not yet been diagnosed with dementia, Merrill said. Healthy lifestyle factors also have been shown to be related to reduced shrinking of the brain and lower rates of atrophy in people with Alzheimer's."The study reinforces the importance of living a healthy life to prevent Alzheimer's, even before the development of clinically significant dementia," Merrill said. 

 Could this be? Fungal infection being the cause of Alzheimer's disease? Noteworthy from this study: all the Alzheimer's disease (AD) patients had evidence of fungal infections in their brains, central nervous systems, and vascular systems, but none were found in the control subjects (those without Alzheimer's disease). Many of the symptoms of AD (such as inflammation of the central nervous system and activation of the immune system) match those with long-lasting fungal infections. A "microbial cause" has long been suggested as a cause of AD, and interestingly other studies have also found fungal infections in AD patients. The research so far has found several fungal species in AD patients (including Candida albicans). The researchers mention that in one study anti-fungal treatment reversed clinical symptoms of AD in 2 patients (but it was written off  as misdiagnosis).

Another possibility that immediately occurs to  explain the findings is that perhaps Alzheimer's disease somehow results in fungal infections - that the AD makes them more prone to fungal infection. In case you're wondering - all the AD patients and control patients studied had died - this is why their brain tissue could be studied so thoroughly. From Nature:

Different Brain Regions are Infected with Fungi in Alzheimer’s Disease

The possibility that Alzheimer’s disease (AD) has a microbial aetiology has been proposed by several researchers. Here, we provide evidence that tissue from the central nervous system (CNS) of AD patients contain fungal cells and hyphae. Fungal material can be detected both intra- and extracellularly using specific antibodies against several fungi. Different brain regions including external frontal cortex, cerebellar hemisphere, entorhinal cortex/hippocampus and choroid plexus contain fungal material, which is absent in brain tissue from control individuals. Analysis of brain sections from ten additional AD patients reveals that all are infected with fungi. Fungal infection is also observed in blood vessels, which may explain the vascular pathology frequently detected in AD patients. Sequencing of fungal DNA extracted from frozen CNS samples identifies several fungal species. Collectively, our findings provide compelling evidence for the existence of fungal infection in the CNS from AD patients, but not in control individuals.

Neurodegenerative diseases constitute a heterogeneous group of disorders of the central nervous system (CNS) that are characterised by a slow and irreversible loss of neuronal functions. The aetiology of primary neurodegenerative diseases, such as Alzheimer’s disease (AD), multiple sclerosis (MS), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), remains largely unknown. A common feature of many neurodegenerative diseases is the presence of aggregates of misfolded proteins (intracellular inclusions) in regions of the CNS that can serve as neuropathological hallmarks for disease diagnosis1,2. ....The prevailing dogma to explain the pathogenesis of AD is that the accumulation of amyloid deposits formed by Aβ pepetide may induce intracellular tangles of tau protein that in turn leads to neuronal death11. However, the so-called “amyloid hypothesis” has been questioned by several findings including the failure of clinical trials aimed to lower amyloid deposits or tau tangles12,13,14. Moreover, many elderly people with normal cognitive function have substantial amyloid burden in their CNS11. At present, there is no therapy to stop or reverse the symptoms of AD.

Aside from cognitive decline, the vast majority of AD patients present clear signs of inflammation and damage to blood vessels15,16. Inflammation of the CNS and immune activation play a major role in the pathophysiology of AD. Indeed, a number of cytokines, such as interleukins (IL-1 and IL-6), tumor necrosis factor α and interferon γ, are elevated in the brain of AD patients, suggesting an increased immune response17,18,19. These observations have led to the speculation that AD has an autoimmune aetiology20. Many investigators have also considered the idea that AD is an infectious disease, or at least that infectious agents constitute a risk factor for AD21,22,23. Accordingly, genetic material from several viruses and bacteria have been reported in brains from AD patients. In particular, herpes simplex type 1 (HSV-1) and Chlamydophila pneumoniae have been suggested as potential aetiological agents of AD. In addition, brain infection by several pathogens may induce amyloid formation24,25,26. Furthermore, Αβ peptide exhibits antimicrobial activity and shows particularly strong inhibitory activity againstCandida albicans27.

Recently, we provided strong evidence for fungal infection in AD patients28,29. Fungal DNA and proteins were found in frozen brain tissue from AD patients, but not from control patient tissue. Moreover, fungal material could be detected intra- and extracellularly in neurons from AD patients. In the present work, we have examined in detail the presence of fungal structures in different regions of the brain of an AD patient by immunohistochemistry. No fungal material was observed in brain tissue from ten control individuals, whereas fungal infection was clearly present in brains from ten additional AD patients. Moreover we were able to amplify fungal DNA from frozen tissue of different AD brain regions. Collectively, our findings provide compelling evidence for the presence of fungal infection in brains from all AD patients analysed.

Because most of the above results were obtained from only one AD patient and one control individual, it was of interest to examine CNS sections from additional AD patients and controls. To this end, we analysed ERH tissue sections from a further ten AD patients and ten controls by double immunostaining with anti-fungal (green) and anti-tubulin (red) antibodies. Notably, fungal infection was evident in all AD patients studied (Fig. 4), whereas no fungal cells were detected in tissue sections from control individuals.... The existence of different fungal morphologies reinforces the idea that several species can be present, supporting the concept of mixed fungal infections. In conclusion, fungal cells and/or hyphae were found in all AD patients analysed although the morphological characteristics may be different for each patient, thus implying that the fungal species present in each patient may also differ.

The majority of AD patients exhibit pathological lesions of the vascular system in the CNS16,36. Up to 90% of AD patients present various cerebrovascular pathologies, including cerebral amyloid angiopathy, microinfarcts, haemorrhages and microvascular degeneration. Accordingly, deposits of amyloid β in the walls of capillaries, small arterioles and medium-size arteries are evident in most AD patients studied..... Fungal cells of different sizes and hyphae were detected inside capillaries and other blood vessels (Fig. 5). Some staining was also evident in the vessel walls, demonstrating that fungal infection can be detected in the neurovascular system. Also, the CP region from patient AD1 (Fig. 5), but not from C1 (Supplementary Figure 6), contained fungal cells and hyphae that immunoreacted with the different anti-fungal antibodies. These results are in good agreement with the notion that several fungal species can infect blood vessels and cause pathological modifications..... In conclusion, fungal structures can be observed also in the vascular system of AD patients.

DNA amplification and sequencing is the most precise approach to determine specific fungal species present in CNS tissues. Because the vast majority of DNA from tissue samples is human, we previously developed a sensitive nested PCR assay to amplify fungal DNA present in very minor amounts....Sequencing of each fragment from the four PCR assays using DNA from patient AD1 revealed a number of fungal species as listed in Table 1. Of note, several species could be detected from the same region, supporting the concept of mixed fungal infection. Conversely, no single fungal species was present in all four regions of the CNS examined. Of note, some of the species detected, such as Malasezzia spp., Phoma and S. cerevisiae, have been previously identified in AD brains40. Significantly, the majority of the species listed in Table 1 are described as human pathogens42,43. The possibility that different fungal species or a combination of species serves as a risk factor or represents the cause of AD might explain the diversity observed in the evolution and severity of clinical symptoms in each AD patient. 

A major goal of AD research is to uncover the precise aetiology of the disease in order to implement adequate therapies to halt or even reverse clinical symptoms. The possibility that AD is a fungal disease, or that fungal infection is a risk factor for the disease, opens new perspectives for effective therapy for these patients. The present findings demonstrate that fungi can be detected in brain tissue from different regions of the AD CNS. In all eleven patients (plus three additional CP samples) described in this study, as well as in four patients previously analysed, there is clear evidence for fungal cells inside neurons or extracellularly29. Therefore, 100% of the AD patients analysed thus far by our laboratory present fungal cells and fungal material in brain sections.....Observations from other laboratories also support the possibility of fungal infections in AD patients. For example, chitin bodies have been found in AD brains44,45. The proposal that chitin-like polysaccharides play a role in the amyloidogenic process and are aberrantly synthesised by neural cells has been suggested46; however, since chitin is a component of the fungal cell wall, it seems possible that these chitin polysaccharides may originate from fungi.... Moreover, antifungal treatment in two patients diagnosed with AD reversed clinical symptoms51,52. The interpretation of these results was that perhaps these patients were misdiagnosed. Interestingly, Aβ peptide has potent antimicrobial activity, particularly against C. albicans27. Accordingly, it might be possible that the presence of a chronic fungal infection in AD CNS triggers the synthesis of Aβ peptide, which in turn leads to amyloid deposits. These reports together with our present findings support the notion that fungal infection may exist in AD.

Proceeding on the assumption that fungi are the aetiological agent of AD, all of the symptoms observed in AD patients can be readily explained. For example, the slow progression of the disease fits well with the chronic nature of fungal infections if they remain untreated. Moreover, inflammation and activation of the immune system may be due to an infectious fungal agent. Disseminated fungal infections can induce cytokine production53,54,55, which can take place years before the onset of cognitive decline as observed in AD. Thus, this disseminated infection may slowly spread to the CNS and synaptic dysfunction and neuronal loss takes place only when the fungal burden in some areas of the CNS is high. It is quite possible that the existence of one fungal infection may facilitate the colonisation by other fungal species that can affect other areas of the CNS, giving rise to mixed fungal infections.

The diversity of fungal species that can affect the CNS, as well as the combinations of these species, may account for the observed differences in the evolution and severity of clinical symptoms found in AD patients. The pathology of the blood vessels observed in most AD patients can also be explained since they can be infected by fungi37,38,39, particularly arteries, where the oxygen content is higher. Finally, the genetic predisposition observed in approximately 2–5% of AD patients can simply be due to their predisposition to acquire fungal infections because the genetic background of each individual is permissive for this56,57. To the best of our knowledge, none of the symptoms established in AD pathology seem incompatible with the concept that AD may be caused by fungi. Moreover, the disappointing results obtained in human clinical trials designed to lower the burden of β-peptide or tau tangles does not support the amyloid cascade hypothesis12,13,14. These findings suggest that the main pathological agent in AD is still unidentified.

The existence of fungal infection in AD patients may be due to its involvement in the aetiology of this disease, but it could also be possible that, for reasons yet unknown, these patients are more prone to this type of infection. The fact that they are elderly and may have a poor adaptive immune response, or possibly changes in the diet and hygiene habits, may contribute to the emergence of fungal infections. It is evident that clinical trials will be necessary to establish a causal effect of fungal infection in AD. There are at present a number of highly effective antifungal compounds with little toxicity58,59,60,61. A combined effort from the pharmaceutical industry and clinicians is needed to design clinical trials to test the possibility that AD is caused by fungal infection.

  Candida albicans (Credit: Josef Reischig, Wikimedia Commons)

 People fear dementia and Alzheimer's disease, because they are progressive diseases that nothing treats successfully. However, in the past year there have been some studies showing improvements with lifestyle changes (not cures, but for some the progression was slowed or showing some improvements). The latest studies found that exercise (especially aerobic execise) had some beneficial effects on those with mild cognitive impairment (MCI), Alzheimer's disease, and vascular cognitive  impairment (VCI): neuropsychiatric improvements, improvements in biomarkers for the disease, and improved blood flow to the brain. From Medscape:

Physical Activity May Help Treat Dementia

New research shows that being physically active not only reduces cognitive decline and improves neuropsychiatric symptoms in patients with dementia but may actually reduce Alzheimer's disease (AD) biomarkers, including amyloid and tau protein in the brain. Exercise could also benefit patients with types of dementia other than AD, another study suggests.Some of this promising new research on exercise was presented at the Alzheimer's Association International Conference (AAIC) 2015. 

Danish researchers had already presented cognition-related results of the multicenter ADEX study ...The intervention consisted of 1 hour of aerobic exercise three times a week for 16 weeks. The control group received usual care..... The analysis found that these [neuropsychiatric] symptoms improved in the 66 patients in the "high exercise"group... The NI is a 12-item questionnaire that rates, among other things, depression, apathy, agitation, hallucinations, irritability, weight loss, and sleep."We saw that the control group got worse; there was a small decline in this group, which you would expect because this is progressive disease," said Steen Hasselbalch, MD, Danish Dementia Research Centre, Copenhagen, Denmark. "But the intervention group remained at the same level and even got a little better, so at end of the intervention there was a significant difference."

The question arises of whether exercise could not just delay worsening of symptoms but actually change brain pathology.The answer, suggests other research, is yes. In a separate study presented at the AAIC 2015, researchers found decreased phosphorylated tau (P tau) in older, previously sedentary persons completing a 6-month regimen of moderate- to high-intensity aerobic exercise.

The study enrolled 70 patients aged 55 to 89 years with prediabetes as well as amnestic mild cognitive impairment (MCI)....We think they are at high, high risk for developing dementia of the Alzheimer's type." These patients were randomly assigned to the aerobic exercise group or to the stretching group. Those in the aerobic group started slowly — 10 minutes of exercise a week — and gradually built the time and intensity up over 6 weeks to the point where they were exercising 45 minutes a day, 4 days a week, at 75% to 85% of their maximum heart rate...."This group had a choice of exercises: treadmill, stationary cycling, elliptical trainer, or preapproved group classes.

The stretching group, whose members could do balance exercises, gentle yoga, and other approved classes in addition to stretching, maintained a maximum heart rate of below 35%. All exercises were adapted to the needs and limitations of individual patients and were done at a local YMCA.

The researchers looked at biomarkers in cerebrospinal fluid (CSF), including P tau protein and amyloid β 42....Most intervention trials don't show such changes in P tau. "But we saw it with exercise and no medications," said Dr. Baker. "Exercise was enough to move a biomarker that indicates the severity of the disease."  It wasn't surprising, she added, that this was true only for older patients. "It may be that before age 70, you have a lot of compensatory mechanisms that help to maintain brain health, and after 70, those start breaking down."

The study also showed that the aerobic activity increased blood flow to the brain...The researchers demonstrated that the increased blood flow was in regions characteristically affected by aging and AD (ie, memory and processing).Cognitive benefits were particularly noteworthy for executive function..."Our brain imaging results are just fantastic; they show some really nice increases in blood flow in the areas of brain that support executive function and areas of the brain that normally show decreased flow for people with MCI, so it's reversing the blood flow detriment in MCI."

AD may not be the only dementia potentially treatable through exercise. Another study discussed at the meeting showed that this intervention may help those with vascular cognitive impairment (VCI)It's the first intervention trial to suggest that exercise can improve cognition in patients with confirmed VCI, said Teresa Liu- Ambrose, PhD, Canada Research Chair, University of British Columbia, Vancouver, Canada, who reported the results.The 6-month study included 71 patients aged 56 to 96 years with mild VCI of varying physical capacities. They were assigned to usual care that included a nutrition component or to an intervention of moderate-intensity walking, 3 times a week for an hour....In a subset of patients who had neuroimaging, there was "evidence of efficiency" in the brain of those who exercised, Dr Liu-Ambrose told Medscape Medical News.

    Recently I've seen a number of published studies that found benefits to someone being bilingual or benefits in learning a new language. Some benefits recently found in bilinguals (or the "billngual advantage"): more gray matter in the executive control area of the brain, 4 to 5 year delay in onset of Alzheimer's symptoms, processing of information more efficiently and more easily, and young bilingual children are more likely to think that everything is learned (while monolinguals more likely to think things are innate). From Science Daily:

Bilinguals of two spoken languages have more gray matter than monolinguals

A new study published in the journal Cerebral Cortex suggests people who speak two languages have more gray matter in the executive control region of the brain...Early on, bilingualism was thought to be a disadvantage because the presence of two vocabularies would lead to delayed language development in children. However, it has since been demonstrated that bilingual individuals perform better, compared with monolinguals, on tasks that require attention, inhibition and short-term memory, collectively termed "executive control."

This "bilingual advantage" is believed to come about because of bilinguals' long-term use and management of two spoken languages. But skepticism still remains about whether these advantages are present, as they are not observed in all studies...."Given this concern, we took a different approach and instead compared gray matter volume between adult bilinguals and monolinguals. We reasoned that the experience with two languages and the increased need for cognitive control to use them appropriately would result in brain changes in Spanish-English bilinguals when compared with English-speaking monolinguals. And in fact greater gray matter for bilinguals was observed in frontal and parietal brain regions that are involved in executive control."

Gray matter of the brain has been shown to differ in volume as a function of people's experiences. A prominent finding of this type was a report that London taxi drivers have more gray matter in brain areas involved in spatial navigation.

What about being bilingual leads to these advantages?....The researchers compared gray matter in bilinguals of American Sign Language (ASL) and spoken English with monolingual users of English...."Unlike the findings for the Spanish-English bilinguals, we found no evidence for greater gray matter in the ASL-English bilinguals," Olulade says. "Thus we conclude that the management of two spoken languages in the same modality, rather than simply a larger vocabulary, leads to the differences we observed in the Spanish-English bilinguals."

Science Daily: Bilingualism delays Alzheimer's manifestation by more than four years

The symptoms of Alzheimer disease (AD) manifest themselves about four to five years later in bilinguals as opposed to monolinguals. In bilinguals, the disease onset was estimated at the age of 77, while in monolinguals, this was at the age of 73.

From Science Daily:  Bilingual brains better equipped to process information

Speaking more than one language is good for the brain, according to new research that indicates bilingual speakers process information more efficiently and more easily than those who know a single language. The benefits occur because the bilingual brain is constantly activating both languages and choosing which language to use and which to ignore, said a researcher.

From Science daily:  Bilingualism changes children's beliefs

Most young children are essentialists: They believe that human and animal characteristics are innate. That kind of reasoning can lead them to think that traits like native language and clothing preference are intrinsic rather than acquired. But a new study suggests that certain bilingual kids are more likely to understand that it's what one learns, rather than what one is born with, that makes up a person's psychological attributes.