How do diet beverages are hazardous to the brain?
People who drink more than two diet beverages a day or had three servings of soda per week showed signs of accelerated brain ageing which is a risk factor for Alzheimer’s disease. The signs include:
Smaller overall brain volume: The size of the brain correlates with intelligence and researchers also found that diet soda drinkers have smaller brain volumes than others
Poorer episodic memory: Some individuals had some trouble recalling the situations, places, and emotions connected to autobiographical memories
Shrunken hippocampus: This is where the brain's emotion, memory, and autonomic nervous system reside, which controls involuntary functions, such as breathing, blood pressure, and heart rate. It was found that people who consumed at least one diet drink per day were three times more likely to have a stroke and to develop dementia as compared to people who did not. A higher risk of brain problems was not associated with regular (non-diet) soft drinks. And the results remained unchanged when other important factors such as gender, diet, smoking, and physical activity were taken into account.
The brain is tricked into thinking it is getting an extra dose of glucose by diet sodas, but ultimately, the trick is on us because the brain adapts to not receiving additional glucose by overcompensating in other ways. Since we know that the gut has a bacterial superhighway that interacts with key neurotransmitters, diet sodas may upset the gut's bacterial jungle—the microbiome—causing unpredictable results.
A team of researchers discovered that cholecystokinin (CCK), a satiety hormone which is highly expressed in memory formation, could, at higher levels, decrease a person's likelihood of developing Alzheimer's disease by 65 per cent, said the study published in the journal Neurobiology of Aging.
CCK is found in both the small intestines and the brain. In the small intestines, CCK allows for the absorption of fats and proteins. In the brain, CCK is located in the hippocampus, which is the memory-forming region of the brain, said Auriel Willette, Assistant Professor at the Iowa State University in the US.
"The regulation of when and how much we eat can have some association with how good our memory is. what we eat and what our body does with it affects our brain.
"It will hopefully help to shed further light on how satiety hormones in the blood and brain affect brain function," Willette said.
The researchers hope this study will encourage others to look into the nutritional aspect of diets, versus just looking at caloric intake.
Also, Alexandra Plagman, who is the lead author and graduate student at the varsity, is currently looking at how diet impacts an individual's CCK levels through researching fasting glucose and ketone bodies.
"By looking at the nutritional aspect, we can tell if a certain diet could prevent Alzheimer's disease or prevent progression of the disease," Plagman said.
Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), the team looked at CCK in 287 people.
People with Alzheimer's tend to wake up tired and their nights become even less refreshing as memory loss and other symptoms worsen.
However, the reason was not fully understood.
The study, led by the Washington University in St. Louis found that older adults who sleep poorly or have less slow-wave sleep -- deep sleep needed to consolidate memories and wake up feeling refreshed -- have higher levels of tau -- a toxic brain protein.
Tau has also been linked to brain damage and cognitive decline.
"Measuring how people sleep may be a non-invasive way to screen for Alzheimer's disease before or just as people begin to develop problems with memory and thinking," said lead author Brendan Lucey, Assistant Professor from the varsity.
Moreover, the findings, published in the journal Science Translational Medicine, showed that it was not the total amount of sleep that was linked to tau, but the slow-wave sleep, which reflects quality of sleep.
The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren't getting as good quality sleep.
"What's interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired," Lucey added.
For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired.
Up to two decades before Alzheimer's symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by decline of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.
The challenge is finding people on track to develop Alzheimer's before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker, the researchers said.
The findings, done on mice, showed that the research could have implications for the treatment of a wide range of diseases, including Alzheimer's, Parkinson's and brain cancer.
"Improving the delivery of drugs to the central nervous system is a considerable clinical challenge," said lead author Maiken Nedergaard from the University of Rochester Medical Center (URMC) in the US.
"The findings of this study demonstrate that the brain's waste removal system could be harnessed to transport drugs quickly and efficiently into the brain," Nedergaard added.
The study taps into the power of the glymphatic system, the brain's unique process of removing waste that was first discovered by Nedergaard in 2012.
It consists of a plumbing system that piggybacks on the brain's blood vessels and pumps cerebral spinal fluid (CSF) through the brain's tissue, flushing away waste.
In the study, published in the journal JCI Insight, the researchers took advantage of the mechanics of the glymphatic system to deliver drugs deep into the brain.
The team administered antibodies directly into CSF. They then injected the animals with hypertonic saline, a treatment frequently used to reduce intracranial pressure on patients with traumatic brain injury.
The saline triggers an ion imbalance which pulls CSF out of the brain. When this occurs, new CSF delivered by the glymphatic system flows in to take its place, carrying the antibodies with it into brain tissue, the team said.
The researchers developed a new imaging system by customising a macroscope to non-invasively observe the proliferation of the antibodies into the brains of the animals.
They believe that this method could be used to not only deliver into the brain large proteins such as antibodies, but also small molecule drugs and viruses used for gene therapies.
The study demonstrated that meningeal lymphatic vessels in the brain play an essential role in maintaining a healthy homeostasis in ageing brains and could be a new target for the treatment.
These vessels drain fluid from the central nervous system into the cervical lymph nodes and dysfunction of that drainage aggravates cognitive decline as well as Alzheimer's disease pathology.
Moreover, when the healthy aged mice were treated with a molecule that increased meningeal lymphatic vessel size and fluid flow within those vessels, the mice showed improved performance on learning and memory tasks.
"As you age, the fluid movement in your brain slows, sometimes to a pace that's half of what it was when you were younger," said Jennifer Munson, Assistant Professor at the Virginia Polytechnic Institute and State University (Virginia Tech), in the US.
"We discovered that the proteins responsible for Alzheimer's actually do get drained through these lymphatic vessels in the brain along with other cellular debris, so any decrease in flow is going to affect that protein build-up," she added.
For the study, published in the journal Nature, the team engineered a hydrogel that can swell those lymphatic vessels.
As a result of the treatment, the bulk flow of fluid in the brain actually increased, and that seemed to have a positive effect on cognitive abilities.
Munson noted that older mice with normal, age-impaired cognitive abilities experienced the biggest gains in memory and learning from the treatment.
"Our results showed that someday this method could be used as a potential treatment to help alleviate the effects not only of Alzheimer's, but also other age-related cognitive ailments," Munson said.
The results showed that ageing, combined with a high fat and high sugar diet, results in increased inflammation and stress in the hippocampus -- responsible for long-term memory -- and prefrontal cortex -- responsible for complex cognitive, emotional and behavioural function.
Both brain regions are thought to be involved in the progression of Alzheimer's disease.
"This study provides novel information in relation to the mechanistic link between obesity and the transition from adulthood to middle age and signalling cascades that may be related to (Alzheimer's) pathology later in life," said researchers, including Rebecca E.K. MacPherson, from the Brock University in Ontario, Canada.
In the study, published in the journal Physiological reports, the team used a mouse model to look at the effects of an obesity-inducing diet on insulin signalling -- the process that tells the body how to use sugar -- and markers of inflammation and cellular stress.
One group of mice received a high-fat, high-sugar diet ("HFS"), while the control group had a normal diet.
Mice with HFS demonstrated significantly higher markers of inflammation, insulin resistance and cellular stress in areas of the hippocampus thought to be involved in the progression of Alzheimer's disease.
The study also revealed that certain areas of the brain respond differently to risk factors associated with Alzheimer's.
"These results add to our basic understanding of the pathways involved in the early progression of (Alzheimer's) pathogenesis and demonstrate the negative effects of a HFS diet on both the prefrontal cortex and hippocampal regions," MacPherson said.
The findings, published in the journal Nature Chemistry, suggests that in the brain, cholesterol acts as a catalyst which triggers the formation of the toxic clusters of the amyloid-beta protein, which is a central player in the development of Alzheimer's disease.
The researchers found that cholesterol, which is one of the main components of cell walls in neurons, can trigger amyloid-beta molecules to aggregate, and their aggregation eventually leads to the formation of amyloid plaques, in a toxic chain reaction that leads to the death of brain cells.
"The levels of amyloid-beta normally found in the brain are about a thousand times lower than we require to observe it aggregating in the laboratory - so what happens in the brain to make it aggregate?" said lead author Michele Vendruscolo, Professor at Centre for Misfolding Diseases, in the University of Cambridge.
For the study, using a kinetic approach, the researchers found in vitro studies that the presence of cholesterol in cell membranes can act as a trigger for the aggregation of amyloid-beta.
Since amyloid-beta is normally present in such small quantities in the brain, the molecules don't normally find each other and stick together. Amyloid-beta does attach itself to lipid molecules, however, which are sticky and insoluble, the researcher said.
In the case of Alzheimer's disease, the amyloid-beta molecules stick to the lipid cell membranes that contain cholesterol.
Once stuck close together on these cell membranes, the amyloid-beta molecules have a greater chance to come into contact with each other and start to aggregate - in fact, the researchers found that cholesterol speeds up the aggregation of amyloid-beta by a factor of 20.
"The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol's role in Alzheimer's disease through the regulation of its interaction with amyloid-beta," Vendruscolo said.
"We're not saying that cholesterol is the only trigger for the aggregation process, but it's certainly one of them," Vendruscolo added.
Pic Source: News Ghana
The brain relies on the perfect coordination of many elements to function properly. If one of those elements is affected, it affects the entire body.
In Alzheimer's disease, damage to specific neurons alter brainwave rhythms causing a loss of cognitive functions.
The inhibitory interneuron is particularly important for managing brain rhythms, said researchers at Gladstone Institutes in the US.
The scientists uncovered the therapeutic benefits of genetically improved interneurons by transplanting them into the brain of a mouse model of Alzheimer's disease.
The inhibitory interneuron controls complex networks between neurons, allowing them to send signals to one another in a harmonised way. They are responsible for the instructions given by the brain.
An imbalance between these two types of neurons creates disharmony and is seen in multiple neurological and psychiatric disorders, including Alzheimer's disease, epilepsy, schizophrenia and autism.
Researchers noted in Alzheimer's mouse models that the inhibitory interneurons do not work properly.
However, when the enhanced by adding a protein called Nav1.1, the interneurons with enhanced function are able to overcome the toxic diseased environment and restore brain function.
They are then able to properly control the activity of excitatory cells and restore brain rhythms, the researchers noted.
"We took advantage of the fact that transplanted interneurons can integrate remarkably well into new brain tissues, and that each interneuron can control thousands of excitatory neurons," said Jorge Palop, Assistant Professor at the University of California in San Francisco, the US.
"These properties make interneurons a promising therapeutic target for cognitive disorders associated with brain rhythm abnormalities and epileptic activity," Palop added, in a paper published in the journal Neuron.
The discovery, published in the Journal of Experimental Medicine, could be the key to stopping damage caused by uncontrolled inflammation in a range of common diseases including liver disease, Alzheimer's and gout.
"Now that we understand how this pathway naturally turns off in health, we can investigate why it does not turn off in disease -- so it's very exciting," said Kate Schroder, Associate Professor at University of Queensland in Australia.
Her work focuses on inflammasomes, which are machine-like protein complexes at the heart of inflammation and disease.
"These complexes form when an infection, injury or other disturbance is detected by the immune system, and they send messages to immune cells to tell them to respond," Schroder said.
"The inflammasome initiates the inflammation process by activating a protein that functions like a pair of scissors, and cuts itself and other proteins," she added.
"What we've found is that after a period of time this protein cuts itself a second time to turn off the pathway, so if we can tweak this system we may be able to turn it off manually in disease," Schroder said.
Schroder's laboratory has begun studying the inflammasome in fatty liver disease, a rapidly growing health issue due to the increasing global incidence of obesity and diabetes.
Alzheimer's disease is a neurodegenerative condition that causes the decline of cognitive function and the inability to carry out daily life activities.
The findings showed that worsening anxiety symptoms in older adults with may be associated with an increase in amyloid beta levels -- a key factor in the development of Alzheimer's disease.
"When compared to other symptoms of depression such as sadness or loss of interest, anxiety symptoms increased over time in those with higher amyloid beta levels in the brain," said lead author Nancy Donovan.
a geriatric psychiatrist at Brigham and Women's Hospital in Boston.
"This suggests that anxiety symptoms could Abe a manifestation of Alzheimer's disease prior to the onset of cognitive impairment" Donovan added.
Previous studies have suggested depression and other neuropsychiatric symptoms as predictors of Alzheimer's disease progression during its "preclinical" phase -- the time during which brain deposits of fibrillar amyloid and pathological tau accumulate in a patient's brain.
This phase can occur more than a decade before a patient's onset of mild cognitive impairment, the researchers noted.
The team examined the association of brain amyloid beta and longitudinal measures of depression and depressive symptoms in 270 cognitively normal, older adults between 62 and 90 years old, with no active psychiatric disorders.
Their findings, published in The American Journal of Psychiatry, suggest that higher brain amyloid beta burden was associated with increasing anxiety symptoms over time in cognitively normal older adults.
As anxiety is common in older people, rising anxiety symptoms may prove to be most useful as a risk marker in older adults with other genetic, biological or clinical indicators of high Alzheimer's risk.
"If further research substantiates anxiety as an early indicator, it would be important for not only identifying people early on with the disease, but also, treating it and potentially slowing or preventing the disease process early on," Donovan said.
In 2015, these diseases comprised of 16.8 per cent of global deaths, according to the report by the Global Burden of Disease (GBD) project published in the journal The Lancet.
The number of global disability adjusted life years (DALYs) increased 7.4 per cent over the past 25 years, while in 2015 they accounted for 10.2 per cent of DALYs worldwide.
"One of the main reasons for the increase in neurological disorders is longer life expectancy," said Vasily Vlassov, Professor at the National Research University Higher School of Economics in Russia.
"People live longer and, accordingly, suffer dementia more often than several decades ago," Vlassov explained, adding "another reason is a growing population".
The most prevalent neurological disorders were tension-type headaches (about 1,500 million cases), migraine (about 1,000 million), medication overuse headaches (about 60 million), and Alzheimer's disease and other dementias (about 46 million cases).
In addition, the rates of communicable neurological disorders, stroke, and Parkinson's are higher in males than females, and the prevalence was higher particularly in children under five, the report said.
The rates of cases per 100,000 was 15.7 per cent higher in Parkinson's, 2.4 per cent in Alzheimer's, 3.1 per cent in motor neuron disease, and 8.9 per cent higher in brain and nervous system cancers.
However, the number of deaths and DALYs per 100,000 people caused by stroke and communicable neurological disorders decreased by 26 and 29.7 per cent respectively between 1990 and 2015, the report noted.
Alzheimer's is a type of dementia that causes problems with memory, thinking and behaviour changes and the disease is rapidly spreading globally. Every three seconds a person falls prey to it.
Experts said at a press briefing on Tuesday held at a hotel in connection with World Alzheimer's Day that the cost to combat the disease globally had surpassed $818 billion.
They said seven per cent of people aged 65 or more were affected by Alzheimer's while up to 15 per cent of those aged 75 or more were likely to be affected by it.
"If the disease is not timely treated, it becomes incurable," Muhammad Wasay, President, Neurology Awareness and Research Foundation (NARF), warned.
He shared an estimate agreed upon by the experts globally that by 2050 people affected with the disease would be over 50 million worldwide and would upset unlimited numbers of families.
"Dementia is also called ancestral disease and is one of the six reasons of deaths."
He said mostly the disease was linked with ageing and, contrary to the prevailing perception, it could be prevented through remedial measures.
"The average age in Pakistan is increasing, thus increasing the risk of the diseases linked with ageing. Alzheimer's is much common among the people who are 65 or older," he said.
He added that though no treatment of Alzheimer's was available, its incidence could be controlled through remedial measures.
Experts said that, due to lack of awareness, people did not understand its symptoms and associated it with old age.
The advantage of the test, known as Polygenic Hazard Score (PHS), is relative to testing only for the well-known genetic variant APOE E4, which has been considered the strongest genetic predictor of whether someone is likely to develop Alzheimer's -- a chronic neurodegenerative disease that usually starts slowly and worsens over time.
However, APOE E4 is only carried by 10 to 15 per cent of the population and recent research suggests that its effects have been overstated, Xinhua news agency reported on Sunday.
Publishing their findings this week in Annals of Neurology, the team, led by researchers at the University of California, San Francisco (UCSF), and the University of California, San Diego, believes that the PHS test could provide risk estimates for the remaining 85 to 90 per cent of people who do not carry at least one copy of APOE E4.
"Beyond APOE E4 by itself, our polygenic hazard score can identify cognitively normal and mildly impaired older folks who are at greatest risk for developing Alzheimer's associated clinical decline over time," Chin Hong Tan from UCSF and the paper's first author was quoted as saying.
Researchers found that PHS test could predict how long it would take for them to progress to Alzheimer's dementia and how steep their cognitive decline would be.
The test enables the researchers to calculate an age-specific risk of developing Alzheimer's based upon each person's share of 31 genetic variants plus APOE E4.
Electroencephalogram (EEG) technology can be used to measure cognitive deficits in people with amnestic mild cognitive impairment (aMCI).
Individuals with aMCI are at twice the risk of others in their age group of progressing to Alzheimer's disease, but currently no conclusive test exists to predict who will develop the disorder.
While mild cognitive impairment (MCI) is the recognised clinical state between healthy aging and Alzheimer's disease, aMCI is a specific type characterised by deficits in episodic memory, the ability to retain new memories such as recent conversations, events, or upcoming appointments.
"We think this might be more sensitive and more specific in pointing out certain cognitive deficits -- in this case semantic memory (or long-term memory) -- than other non-EEG methods available, because EEG reflects direct neural activity," said study lead author Hsueh-Sheng Chiang, post-doctoral fellow at University of Texas Southwestern Medical Centre in the US.
The study was published in the Journal of Alzheimer's Disease. The study involving 16 individuals with aMCI and 17 age matched healthy controls, the researchers identified a specific variation in brain waves of individuals with aMCI.
The results depicted a pattern of delayed neural activity that is directly related to the severity of impairment in cognitive performance on a word finding task and may indicate an early dysfunction of progression to Alzheimer's disease.
The participants were monitored by EEG and presented with pairs of words that either described features of an object or were randomly paired.
The study reveals a direct link between the main culprit of Alzheimer's disease and memory loss. Alzheimer's disease is characterized by the formation of amyloid plaques in the brain tissue.
These amyloid plaques are made up of an insoluble protein, 'Amyloid-beta' (Abeta), which forms small structures called 'oligomers' that are important in the disease progression.
Although these proteins are known to be involved in Alzheimer's, little is understood about how they lead to memory loss. Neuroscience researchers have investigated how Abeta affected healthy brains of pond snails (Lymnaea stagnalis) by observing the effect of administering the protein following a food-reward training task.
"Because we understand the memory pathways so well, the simple snail brain has provided the ideal model system to enable us to link the loss of established memory to pure Abeta," said George Kemenes, a neuroscientist at the University of Sussex.
Snails treated with Abeta had significantly impaired memories 24 hours later when tested with the food task, even though their brain tissue showed no sign of damage.
"This demonstrated that Abeta alone is enough to lead to the symptoms of memory loss that are well known in Alzheimer's disease," said lead author Lenzie Ford from the University of Sussex.
The work will provide a platform for a more thorough investigation of the mechanisms and effects on memory pathways that lead to this memory loss.
"It is absolutely essential that we understand how Alzheimer's disease develops in order to find specific targets for therapeutics to combat this disease," said professor Serpell, who is senior author on the study.
The study appeared in the journal Scientific Reports.
According to the researchers, the green tea extract, epigallocatechin-3-gallate (EGCG), which was found effective in mice could lead to advancements in the treatment and prevention of Alzheimer's in humans too.
"In Alzheimer's patients, amyloid-beta peptide (A-beta) can accumulate and clump together causing amyloid plaques in the brain," said Todd Schachtman, professor of psychological sciences in the College of Arts and Science at University of Missouri.
Symptoms can include increased memory loss and confusion, agitation and a lack of concern for your environment and surroundings.
"We looked at ways of preventing or postponing the onset of the disease which we hope can eventually lead to an improvement of health status and quality of life for the elderly," Schachtman noted.
The researchers decided to investigate the effects of voluntary exercise and EGCG on memory function and A-beta levels in mice known to show plaque deposits and behaviour deficits.
Researchers administered EGCG in the drinking water of the mice and gave them access to running or exercise wheels.
The researchers found remarkable improvements in the cognitive function and retention in the Alzheimer's affected mice that were given EGCG and were allowed to exercise.
"Oral administration of the extract, as well as voluntary exercise, improved some of the behavioural manifestations and cognitive impairments of Alzheimer's," Grace Sun, professor emerita of biochemistry at MU, noted.
The findings appeared in the Journal of Alzheimer's Disease.
The present study, published in the Journal of Alzheimer's Disease, stands in contrast to the previous research that found a correlation between smoking and dementia.
"The underlying data (in those studies) was solid, but the analysis didn't take into account the idea of competing risk of mortality, which we felt was an important factor to consider in this case since smoking is so strongly associated with earlier death," Erin Abner from University of Kentucky, who was among the the researchers, said.
For the study, the researchers included 531 initially cognitively-normal people.
They used a statistical method called competing risk analysis to determine whether there was a connection between smoking and dementia.
The data demonstrated that smoking was associated with a risk of earlier death -- but not dementia.
"While our study results could influence smoking cessation policy and practice, we feel that the most important consequence of our work is to demonstrate how this method could change the way we approach dementia research and to advocate for its adoption in the appropriate areas of study," said Abner.
"To be clear, we are absolutely not promoting smoking in any way.
"We're saying that smoking doesn't appear to cause dementia in this population," Abner added.
Using current techniques, Alzheimer's disease, the most frequent cause of dementia, can only be detected once the typical plaques have formed in the brain.
At this point, therapy seems no longer possible. However, the first changes caused by Alzheimer's take place on the protein level up to 20 years sooner.
"Once amyloid plaques have formed, it seems that the disease can no longer be treated," said study co-author Andreas Nabers from Ruhr-University Bochum in Germany.
In Alzheimer's patients, the amyloid beta protein folds incorrectly due to pathological changes long before the first symptoms occur.
A team of researchers headed by Klaus Gerwert from Ruhr-University Bochum successfully diagnosed this misfolding using a simple blood test. As a result, the disease could be detected approximately eight years before the first clinical symptoms occur.
But experiments showed that the test was not suitable for clinical applications as the test provided false positive diagnoses for nine per cent of the study participants.
In order to increase the number of correctly identified Alzheimer's cases, the researchers have now introduced the two-tier diagnostic method.
To this end, they use the original blood test to identify high-risk individuals. Subsequently, they add a dementia-specific biomarker, namely tau protein, to run further tests with those test participants whose Alzheimer's diagnosis was positive in the first step.
If both biomarkers show a positive result, there is a high likelihood of Alzheimer's disease, said the study published in the journal Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring.
"Through the combination of both analyses, 87 of 100 Alzheimer's patients were correctly identified in our study," Gerwert said.
"Now, new clinical studies with test participants in very early stages of the disease can be launched," Gerwert added.
"Our research shows that in a late-middle-age population at risk for Alzheimer's disease, physically active individuals experience fewer age-related alterations in biomarkers associated with the disease, as well as memory and cognitive functioning," said Ozioma Okonkwo, Assistant Professor at the University of Wisconsin.
For the results, the research team conducted three studies--in the first study, the researchers examined 317 participants enrolled in the Wisconsin Registry for Alzheimer's Prevention, an ongoing observational study of more than 1,500 people with a history of parents with probable Alzheimer's dementia.
In the second study, researchers studied 95 people, also from the registry, who were given scores called polygenic risk scores, based on whether they possessed certain genes associated with Alzheimer's.
Similarly, the third study examined MRIs from 107 individuals from the registry who were asked to run on a treadmill to determine their oxygen uptake efficiency slope, a measure of aerobic fitness.
Participation in the registry included an initial assessment of biological, health and lifestyle factors associated with the disease and follow-up assessments every two to four years.
All participants completed a questionnaire about their physical activity and underwent neuropsychological testing and brain scans to measure several biomarkers associated with Alzheimer's disease.
The researchers compared data from individuals younger than 60 years with older adults and found a decrease in cognitive abilities as well as an increase in biomarkers associated with the disease in older individuals.
However, the effects were significantly weaker in older adults who reported engaging in the equivalent of at least 30 minutes of moderate exercise five days a week.
"The most interesting part of our research is that we now show evidence that lifestyle habits - in this case regular, moderate exercise - can modify the effect of what is commonly considered a non-modifiable risk factor for Alzheimer's, in this case, aging," Okonkwo said.
"Overall, these studies suggest that the negative effect of aging and genetic risk on Alzheimer's' disease biomarkers and cognition can be lessened in physically active, older adults at risk for the disease compared with their less active peers."
Preclinical research published in the Journal of Pharmacology and Experimental Therapeutics found that the drug -- called BPN14770 -- deters the effects of amyloid beta, a hallmark protein of Alzheimer's that is toxic to nerve cells.
BPN14770, under development by Tetra Therapeutics, could help activate these mechanisms that support nerve health and prevent dementia, even with the progression of Alzheimer's.
"Such observations imply that Alzheimer's pathology can be tolerated by the brain to some extent due to compensatory mechanisms operating at the cellular and synaptic levels," said study researcher Ying Xu, Associate Professor at University at Buffalo.
"Our new research suggests that BPN14770 may be capable of activating multiple biological mechanisms that protect the brain from memory deficits, neuronal damage and biochemical impairments," Xu added.
The research conducted in mice, discovered that BPN14770 inhibits the activity of phosphodiesterase?4D (PDE4D), an enzyme that plays a key role in memory formation, learning, neuroinflammation and traumatic brain injury.
PDE4D lowers cyclic adenosine monophosphate (cAMP) -- a messenger molecule that signals physiological changes such as cell division, change, migration and death -- in the body, leading to physical alterations in the brain.
cAMP has numerous beneficial functions, including improved memory. By inhibiting PDE4D, BPN14770 increases cAMP signalling in the brain, which ultimately protects against the toxic effects of amyloid beta.
"The role of PDE4D in modulating brain pathways involved in memory formation and cognition, and the ability of our PDE4D inhibitor to selectively enhance this process, has been well studied," said Mark E. Gurney from Tetra Therapeutics.
"We are very excited by our colleagues' findings, which now suggest a second protective mechanism of action for BPN14770 against the progressive neurological damage associated with Alzheimer's disease," Gurney said.
"Developing effective drugs for memory deficits associated with Alzheimer's disease has been challenging," said M. O'Donnell, Professor at University at Buffalo.
"BPN14770 works by a novel mechanism to increase cyclic AMP signalling in the brain, which has been shown to improve memory. The collaborative project has led to clinical trials that will begin to test its effectiveness," O'Donnell said.
According to the study published in the journal Canadian Medical Association Journal (CMAJ), using donepezil increases the risk of hospital admission for rhabdomyolysis, a painful condition of muscle breakdown, compared with several other cholinesterase inhibitors.
Dementia is a growing problem, with almost 10 million newly diagnosed cases every year around the world, said the researchers.
"The findings of this population-based cohort study support regulatory agency warnings about the risk of donepezil-induced rhabdomyolysis," said study researcher Jamie Fleet from McMaster University in Canada.
The study, led by researchers at Western University, looked at ICES data from 2002 to 2017 on 2,20,353 patients aged 66 years or older in Ontario, Canada, with a new prescription for donepezil, rivastigmine or galantamine, three cholinesterase inhibitors used to manage dementia and Alzheimer disease.
The researchers found that donepezil was associated with a two-fold higher risk of hospitalisation for rhabdomyolysis, a serious condition that can result in kidney disease.
According to the findings, the relative risk was small but statistically significant.
"This is the first study to really show, in a statistical model, that air pollution was associated with changes in people's brains and that those changes were then connected with declines in memory performance," said study researcher Andrew Petkus, Assistant Professor University of South California in US.
Previous research has suggested that fine particle pollution exposure increases the risk for Alzheimer's disease and related dementias.
What scientists haven't known is whether PM2.5 alters brain structure and accelerates memory decline.
For the study, published in the journal Brain, researchers used data from 998 women, aged 73 to 87, who had up to two brain scans five years apart as part of the landmark Women's Health Initiative launched in 1993 by the US National Institutes of Health and enrolled more than 160,000 women to address questions about heart disease, cancer and osteoporosis.
Those brain scans were scored on the basis of their similarity to Alzheimer's disease patterns by a machine learning tool that had been "trained" via brain scans of people with Alzheimer's disease.
The researchers also gathered information about where the 998 women lived, as well as environmental data from those locations to estimate their exposure to fine particle pollution.
When all that information was combined, researchers could see the association between higher pollution exposure, brain changes and memory problems - even after adjusting to taking into account differences in income, education, race, geographic region, cigarette smoking and other factors.
"This study provides another piece of the Alzheimer's disease puzzle by identifying some of the brain changes linking air pollution and memory decline. Each research study gets us one step closer to solving the Alzheimer's disease epidemic," Petkus said.
"Our hope is that by better understanding the underlying brain changes caused by air pollution, researchers will be able to develop interventions to help people with or at risk for cognitive decline," Petkus added.
The team from Pohang University of Science and Technology (POSTECH) in South Korea developed a wireless powered smart contact lens that can diagnose and treat diabetes by controlling drug delivery with electrical signals.
The smart contact lens was able to effectively monitor blood sugar or glucose levels.
The contact lenses are made of biocompatible polymers and integrate biosensors and drug delivery and data communication systems, according to the study, published in the journal Science Advances.
"Despite the full-fledged research and development of wearable devices from global companies, the commercialisation of wireless-powered medical devices for diagnosis and treatment of diabetes and retinopathy is insufficient," said study lead researcher Sei Kwang Han from POSTECH.
"We expect that this research will greatly contribute to the advancement of related industries by being the first in developing wireless-powered smart contact lenses equipped with drug delivery system for diagnosis and treatment of diabetes, and treatment of retinopathy, he added.
According to the findings, the research team verified that the glucose level in tears of diabetic rabbits analysed by smart contact lenses matched their blood glucose level using a conventional glucose sensor that utilises drawn blood.
The team additionally confirmed that the drugs encased in smart contact lenses could treat diabetic retinopathy.
Recently, by applying the platform technology of these smart contact lenses, research has been conducted to expand the scope of electroceuticals that use electrical stimulations to treat brain disorders such as Alzheimer's and mental illnesses including depression, the authors said.
The research team expects this development of self-controlled therapeutic smart contact lenses with real-time biometric analysis to be quickly applied to wearable healthcare industries.
The research team is preparing to carry out clinical trials for the safety and validity assessment for commercialisation of smart contact lenses in collaboration with Interojo Inc., a Korea-based company engaged in the manufacture and marketing of contact lenses.
(IANS)
"Because there are no treatments for Alzheimer's disease, it is crucial that we find ways to prevent it and delay its onset," said study researcher Albert Amran from the University of Texas Health Science Centre in the US.
"About 5.8 million people in the US have this disease, so even a small reduction in risk can make a dramatic difference. We began our study by looking for ways we could reduce this risk," Amran added.
The aim of the researchers was to pinpoint potential factors that could reduce Alzheimer's disease risk.The role was to sort through enormous amounts of de-identified patient data in the Cerner Health Facts database to see whether there are drugs that could be repurposed to reduce the risk of Alzheimer's disease.
Once the team identified the flu vaccine as a candidate, they used machine learning to analyse more than 310,000 health records to study the relationship between flu vaccination and Alzheimer's disease. The study found that more frequent flu vaccination and receiving a vaccination at younger ages were associated with even greater decreases in risk.
"One of our theories of how the flu vaccine may work is that some of the proteins in the flu virus may train the body's immune response to better protect against Alzheimer's disease," Amran said.
"Providing people with a flu vaccine may be a safe way to introduce those proteins that could help prepare the body to fight off the disease," he added.
The researchers noted that additional studies in large clinical trials are needed to explore whether the flu shot could serve as a valid public health strategy in the fight against this disease.
"More research is needed to investigate why and how the flu vaccine works in the body to help prevent Alzheimer's disease," the authors wrote.
The study was presented at the 2020 Alzheimer's Association International Conference on July 27-31. The conference was held virtually due to Covid-19.
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