Alzheimer Archives - Iran News Daily

Aerobic Exercise Slows the Risk of Alzheimer’s

reporter 1222 — Sun, 06 Oct 2019 09:00:13 +0000

Tehran (Iran News) – A new study suggests that regular weekly aerobic exercise may slow or prevent cognitive decline in older adults who are at a high risk of developing Alzheimer’s.

“This is the first randomized and controlled trial … to assess effects of exercise on brain structure, function and amyloid burden in older adults who have memory problems, thus, high risks of Alzheimer’s disease,” said lead author Rong Zhang, a neurology professor at UT Southwestern Medical Center, Iran News quotes what CNN reported.

The study was a small proof-of-concept trial of people ages 55 and older with mild cognitive impairment. Subjects were randomized to 12 months of aerobic exercise or stretching and toning. Both aerobic and stretching may prevent or slow cognitive decline, according to the researchers, but aerobic exercise had more benefits on reducing hippocampal shrinkage than stretching. The hippocampus is a region of the brain crucial for memory.

Neither type of exercise prevented amyloid clumps — a hallmark of Alzheimer’s disease — from continuing to develop in the brains of the 70 adults who participated in the study. But MRI and PET imaging showed those who did aerobic exercise had slower degeneration in the hippocampus than those who did flexibility training.

“The brains of participants with amyloid responded more to the aerobic exercise than the others,” Zhang said.

“The key positive finding is that the exercise intervention specifically reduced shrinkage of the memory center in the brain in people with the earliest symptomatic stage of Alzheimer’s disease,” said neurologist Dr. Richard Isaacson, who founded the Alzheimer’s Prevention Clinic at Weill Cornell Medicine.

“Most physicians believe in the power of exercise to support overall brain health, but fewer believe that exercise can specifically impact people with early Alzheimer’s,” Isaacson said. “This study brings us one step closer toward teasing out the effects in people with biomarker defined Alzheimer’s.”

While the study results must be replicated in much larger studies, Zhang suggested that anyone concerned about cognitive decline or Alzheimer’s consider adding exercise to their daily lives. While it’s best to start exercising early in life, he said, “it is not too late to receive the benefits of exercise even late in life when there are already amyloid clumps in the brain.”

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Alzheimer’s Brain Damage Could Be Accelerated by Sleep Deprivation

reporter 1222 — Fri, 25 Jan 2019 11:21:18 +0000

Researchers have understood little about how sleep disruptions drive the disease, but now by studying mice and people they found that sleep deprivation increases levels of the key Alzheimer’s protein tau.

In follow-up studies in the mice, the research team at Washington University School of Medicine in St. Louis has shown that sleeplessness accelerates the spread through the brain of toxic clumps of tau - a harbinger of brain damage and decisive step along the path to dementia.

These findings, published online Jan. 24 in the journal Science, indicate that lack of sleep alone helps drive the disease, and suggests that good sleep habits may help preserve brain health, Medical Xpress reported.

“The interesting thing about this study is that it suggests that real-life factors such as sleep might affect how fast the disease spreads through the brain,” said senior author David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. “We’ve known that sleep problems and Alzheimer’s are associated in part via a different Alzheimer’s protein—amyloid beta—but this study shows that sleep disruption causes the damaging protein tau to increase rapidly and to spread over time.”

Tau is normally found in the brain—even in healthy people—but under certain conditions it can clump together into tangles that injure nearby tissue and presage cognitive decline. Recent research at the School of Medicine has shown that tau is high in older people who sleep poorly. But it wasn’t clear whether lack of sleep was directly forcing tau levels upward, or if the two were associated in some other way. To find out, Holtzman and colleagues including first authors Jerrah Holth, Ph.D., a staff scientist, and Sarah Fritschi, Ph.D., a former postdoctoral scholar in Holtzman’s lab, measured tau levels in mice and people with normal and disrupted sleep.

Mice are nocturnal creatures. The researchers found that tau levels in the fluid surrounding brain cells were about twice as high at night, when the animals were more awake and active, than during the day, when the mice dozed more frequently. Disturbing the mice’s rest during the day caused daytime tau levels to double.

Much the same effect was seen in people. Brendan Lucey, MD, an assistant professor of neurology, obtained cerebrospinal fluid—which bathes the brain and spinal cord—from eight people after a normal night of sleep and again after they were kept awake all night. A sleepless night caused tau levels to rise by about 50 percent, the researchers discovered.

Staying up all night makes people stressed and cranky and likely to sleep in the next chance they get. While it’s hard to judge the moods of mice, they, too, rebounded from a sleepless day by sleeping more later. To rule out the possibility that stress or behavioral changes accounted for the changes in tau levels, Fritschi created genetically modified mice that could be kept awake for hours at a time by injecting them with a harmless compound. When the compound wears off, the mice return to their normal sleep-wake cycle—without any signs of stress or apparent desire for extra sleep.

Using these mice, the researchers found that staying awake for prolonged periods causes tau levels to rise. Altogether, the findings suggest that tau is routinely released during waking hours by the normal business of thinking and doing, and then this release is decreased during sleep allowing tau to be cleared away. Sleep deprivation interrupts this cycle, allowing tau to build up and making it more likely that the protein will start accumulating into harmful tangles.

In people with Alzheimer’s disease, tau tangles tend to emerge in parts of the brain important for memory—the hippocampus and entorhinal cortex—and then spread to other brain regions. As tau tangles mushroom and more areas become affected, people increasingly struggle to think clearly.

To study whether the spread of tau tangles is affected by sleep, the researchers seeded the hippocampi of mice with tiny clumps of tau and then kept the animals awake for long periods each day. A separate group of mice also was injected with tau tangles but was allowed to sleep whenever they liked. After four weeks, tau tangles had spread further in the sleep-deprived mice than their rested counterparts. Notably, the new tangles appeared in the same areas of the brain affected in people with Alzheimer’s.

“Getting a good night’s sleep is something we should all try to do,” Holtzman said. “Our brains need time to recover from the stresses of the day. We don’t know yet whether getting adequate sleep as people age will protect against Alzheimer’s disease. But it can’t hurt, and this and other data suggest that it may even help delay and slow down the disease process if it has begun.”

The researchers also found that disrupted sleep increased release of synuclein protein, a hallmark of Parkinson’s disease. People with Parkinson’s—like those with Alzheimer’s—often have sleep problems.

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Eye exam may predict Alzheimer’s

reporter 1222 — Fri, 24 Aug 2018 08:15:12 +0000

Advances in eye exam technology could one day help doctors diagnose people with Alzheimer’s disease long before symptoms appear, researchers said Thursday.

Using equipment similar to the kind already available at most eye doctors’ offices, researchers detected signs of Alzheimer’s in a small sample of 30 people, according to a study published in the Journal of the American Medical Association (JAMA) Opthalmology.

Those enrolled in the study — all in their mid-70s with no outward symptoms of Alzheimer’s — underwent PET scans or sampling of spinal fluid.

About half came back with elevated levels of the Alzheimer’s proteins amyloid or tau, suggesting they would eventually develop dementia.

In this group, researchers also found thinning in the retina, something that experts had previously seen in autopsies of people who died from Alzheimer’s disease.

“In the patients with elevated levels of amyloid or tau, we detected significant thinning in the center of the retina,” said co-principal investigator Rajendra Apte, professor of ophthalmology and visual sciences at Washington University in St. Louis.

“All of us have a small area devoid of blood vessels in the center of our retinas that is responsible for our most precise vision. We found that this zone lacking blood vessels was significantly enlarged in people with preclinical Alzheimer’s disease.”

The study did not, however, reveal if the participants with thinning retinas went on to develop Alzheimer’s or not.

For that reason, Doug Brown, chief policy and research Officer, Alzheimer’s Society, called the area of research “fascinating” but sounded a note of caution.

“Without confirming that any of the people with preclinical Alzheimer’s actually went on to develop the disease, we would need to see this carried out on a much larger group over a longer period of time to draw any firm conclusions,” said Brown, who was not involved in the study.

Sara Imarisio, head of research at Alzheimer’s Research UK, agreed.

“While the eye tests used in this research are relatively quick, inexpensive and non-invasive, as only 30 people took part in the study, we still need to see more research before we can tell how useful this method could be for highlighting early signs of Alzheimer’s”

– Dementia on rise –

Experts say brain damage from Alzheimer’s disease can begin up to two decades before signs of memory loss appear.

Close to 50 million people are living with dementia around the globe, and the toll is expected to mount in the coming decades as the population ages.

Alzheimer’s is the most common form of dementia, and there is no cure. But earlier detection may make it possible for drug or lifestyle interventions that may stave off the disease.

Currently, doctors use PET scans and lumbar punctures to help diagnose Alzheimer’s — both expensive and invasive techniques.

The type of technology used in the JAMA study is called optical coherence tomography angiography (OCT-A).

It is commonly used to shine light into the eye so that a doctor can measure the thickness of the retina and optic nerve.

Researchers say the retina and central nervous system are interconnected, so changes in the brain can be reflected in the cells of the retina.

“This technique has great potential to become a screening tool that helps decide who should undergo more expensive and invasive testing for Alzheimer’s disease prior to the appearance of clinical symptoms,” said the study’s first author Bliss E. O’Bryhim, a resident physician in the Department of Ophthalmology and Visual Sciences at Washington University.

The study authors agree that more work is needed to confirm if the technique works in larger populations, but are hopeful that it could one day help screen people in their 40s and 50s.

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Study Warns: Powerful Sleeping Pills Raise Risk of Alzheimer’s

reporter 1222 — Thu, 16 Aug 2018 08:00:30 +0000

Researchers found the risk of developing the memory-robbing disorder is higher for patients taking benzodiazepines and Z-drugs.

And the huge analysis revealed a higher risk for those on stronger medications, and for those who have taken the drugs for longer than recommended.

Figures suggest there are at least 260,000 people in Britain and nearly 100 million in the US who take benzodiazepines and Z-drugs for at least a month, Daily Mail reported.

The recommended usage of benzos and Z-drugs is no more than four weeks, as evidence suggests they do little after this time.

Doctors dole out benzos, which slow the body’s functions and are highly effective in the short-term, to combat anxiety and sleeplessness.

Z-drugs are hypnotic sedatives that work similarly to benzos. The most well-known are zolpidem, zopiclone and zaleplon.

Evidence is growing over benzos – a class of powerful sedatives, which include Valium and Xanax – and their links to dangerous addiction.

And the new study, carried out by the University of Eastern Finland, if confirmed in further trials, may add to the long-list of dangers, including falls and even an early death.

Researchers analysed the use of benzodiazepines and Z-drugs and the prevalence of Alzheimer’s among 353,000 participants.

Of the participants, a fifth had already given the devastating news they had the most common form of dementia between 2005 and 2011.

Medical records of each participant since 1995 were collected, to examine any links between medication use and the disorder.

For patients taking benzodiazepines or Z-drugs, the risk of Alzheimer’s increased by around six per cent, according to an analysis.

Researchers led by Vesa Tapiainen also found the higher the dose, the more likely the patient was to be struck down with the disorder.

Mr Tapiainen and colleagues admitted the increased risk of Alzheimer’s was small.

The findings of the Finnish trial were published in the journal Acta Psychiatrica Scandinavica.

Writing in the journal, researchers said: ‘Benzodiazepine and related drug use in general was associated with modestly increased risk of Alzheimer’s.’

For decades, patient groups, addiction charities and experts have warned about the over-use of benzodiazepines.

Studies have shown people who take the powerful sedatives for six weeks face a 50 per cent chance of becoming addicted.

And once hooked, the only help thousands can receive is from addiction services on the NHS that are often frequented by Class A drug addicts.

Concerned charities have also called for doctors to change prescribing habits but such calls have been largely ignored.

Withdrawal symptoms for patients coming off benzodiazepines can include anxiety, panic attacks and even hallucinations.

Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: ‘This study suggests that taking drugs such as benzodiazepines maybe associated with a slightly increased risk of developing Alzheimer’s, but the results don’t give conclusive evidence about what causes this link.

‘While this study only looked at benzodiazepine use more than five years before people were diagnosed with Alzheimer’s, we know that the disease can start to get underway in the brain up to twenty years before obvious memory and thinking symptoms start to show.

‘Benzodiazepines are often prescribed to treat sleep problems or anxiety, and as these symptoms may also be early indicators of the onset of Alzheimer’s, this could account for the link highlighted in this study.

‘These drugs need to be carefully prescribed and doctors are best placed to assess individual circumstances, weigh benefits against any potential risks and to make an informed judgement about the most appropriate course of treatment.’

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‘Big Bang’ of Alzheimer’s: Genesis of Disease

reporter 1222 — Mon, 16 Jul 2018 07:10:10 +0000

Scientists have discovered a ‘Big Bang’ of Alzheimer’s disease — the precise point at which a healthy protein becomes toxic but has not yet formed deadly tangles in the brain.

A study from UT Southwestern’s O’Donnell Brain Institute provides novel insight into the shape-shifting nature of a tau molecule just before it begins sticking to itself to form larger aggregates. The revelation offers a new strategy to detect the devastating disease before it takes hold and has spawned an effort to develop treatments that stabilize tau proteins before they shift shape.

“We think of this as the Big Bang of tau pathology. This is a way of peering to the very beginning of the disease process.”

Dr. Mark Diamond, Director for UT Southwestern’s Center for Alzheimer’s and Neurodegenerative Diseases “This is perhaps the biggest finding we have made to date, though it will likely be some time before any benefits materialize in the clinic. This changes much of how we think about the problem,” said Dr. Marc Diamond, Director for UT Southwestern’s Center for Alzheimer’s and Neurodegenerative Diseases and a leading dementia expert credited with determining that tau acts like a prion — an infectious protein that can self-replicate.

The study published in eLife contradicts the previous belief that an isolated tau protein has no distinct shape and is only harmful after it begins to assemble with other tau proteins to form the distinct tangles seen in the brains of Alzheimer’s patients.

Scientists made the discovery after extracting tau proteins from human brains and isolating them as single molecules. They found that the harmful form of tau exposes a part of itself that is normally folded inside. This exposed portion causes it to stick to other tau proteins, enabling the formation of tangles that kill neurons.

“We think of this as the Big Bang of tau pathology,” said Dr. Diamond, referring to the prevailing scientific theory about the formation of the universe. “This is a way of peering to the very beginning of the disease process. It moves us backward to a very discreet point where we see the appearance of the first molecular change that leads to neurodegeneration in Alzheimer’s. This work relied on a close collaboration with my colleague, Dr. Lukasz Joachimiak.”

Despite billions of dollars spent on clinical trials through the decades, Alzheimer’s disease remains one of the most devastating and baffling diseases in the world, affecting more than 5 million Americans alone.

Dr. Diamond is hopeful the scientific field has turned a corner, noting that identifying the genesis of the disease provides scientists a vital target in diagnosing the condition at its earliest stage, before the symptoms of memory loss and cognitive decline become apparent.

His team’s next steps are to develop a simple clinical test that examines a patient’s blood or spinal fluid to detect the first biological signs of the abnormal tau protein. But just as important, Dr. Diamond said, efforts are underway to develop a treatment that would make the diagnosis actionable.

He cites a compelling reason for cautious optimism: Tafamidis, a recently approved drug, stabilizes a different shape-shifting protein called transthyretin that causes deadly protein accumulation in the heart, similar to how tau overwhelms the brain.

“The hunt is on to build on this finding and make a treatment that blocks the neurodegeneration process where it begins,” Dr. Diamond said. “If it works, the incidence of Alzheimer’s disease could be substantially reduced. That would be amazing.”

Dr. Diamond’s lab, at the forefront of many notable findings relating to tau, previously determined that tau acts like a prion — an infectious protein that can spread like a virus through the brain. The lab has determined that tau protein in the human brain can form many distinct strains, or self-replicating structures, and developed methods to reproduce them in the laboratory. He said his newest research indicates that a single pathological form of tau protein may have multiple possible shapes, each associated with a different form of dementia.

Dr. Diamond, who holds the Distinguished Chair in Basic Brain Injury and Repair, is founding Director of the Center for Alzheimer’s and Neurodegenerative Diseases, and Professor of Neurology & Neurotherapeutics with the Peter O’Donnell Jr. Brain Institute at UT Southwestern. He collaborated on the study with co-corresponding author Dr. Joachimiak, an Assistant Professor in the Center for Alzheimer’s and Neurodegenerative Diseases and an Effie Marie Cain Scholar in Medical Research.

The research was supported with funding from the Rainwater Charitable Foundation, the National Institutes of Health, and the Effie Marie Cain Endowed Scholarship.

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Alzheimer’s Disease Gene Successfully Removed From Human Brain

reporter 1222 — Mon, 16 Apr 2018 07:30:31 +0000

Scientists were able to successfully remove a gene that caused Alzheimer’s disease from the human brain, possibly paving the way for a new kind of treatment against the dreaded illness.

There have been numerous proposals on a possible treatment or cure for Alzheimer’s disease, including an enzyme inhibitor and frontal lobe stimulation. This one is different though, primarily because the tests were carried out not on laboratory mice, but on humans.

Scientists from the Gladstone Institutes, a San Francisco-based independent biomedical research institution, were able to remove the primary genetic risk factor for Alzheimer’s disease, which is a gene named apoE4, Techtime reported.

In their findings, published in the Nature Medicine journal, the researchers found that human brains that possess even one copy of apoE4 are over twice as likely to eventually develop Alzheimer’s disease within their lifetime. In addition, brains that have two copies of the gene carry an increased risk by 12 times.

The researchers created neurons from the skin cells of Alzheimer’s disease patients that have two copies of the apoE4 gene, and of healthy individuals that have two copies of the apoE3 gene. The scientists discovered that the apoE4 protein is not able to properly function in human neurons, and is broken down into fragments.

This leads to several problems that are commonly found among victims of Alzheimer’s disease, including the formation of beta-amyloid protein. Excessive beta-amyloids may clump together to create plaques, which disrupt neurons and result in symptoms that are associated with the illness.

The findings came as a surprise to the researchers because in previous studies where mice were used for Alzheimer’s disease research, the apoE4 gene did not result in increased beta-amyloid levels.

To repair the abnormalities in the human brain caused by the apoE4 gene, the researchers created compounds that transformed the apoE4 protein into the harmless apoE3 protein. These so-called structure correctors eliminated all the possible signs for Alzheimer’s disease, and the researchers are now looking to further improve the compounds to prepare for human testing in the future.

According to Yadong Huang, the lead author of the study, the development of an Alzheimer’s disease cure has been “largely a disappointment” in the past decade, with many drugs working in mice but failing in clinical trials with humans. With this new research tested on humans and not mice, this may be science’s best shot at finding the elusive Alzheimer’s disease cure.

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5 Ways to Reduce Your Risk of Alzheimer’s Disease

reporter 1222 — Thu, 05 Apr 2018 06:50:54 +0000

According to the Alzheimer’s Association, “Today, someone in the United States develops Alzheimer’s every 65 seconds. By mid-century, someone in the United States will develop the disease every 33 seconds.”

To date, there is no cure regarding this most common form of dementia, which affects nearly all individuals worldwide regardless of race, or socioeconomic status, a trend that continues to grow at a disturbingly alarming rate. Scientists however are close to identifying contributing factors that may hinder or help the progression of this illness in the long run.

Listed below are the top 5 factors that can contribute to this disheartening condition, including some that haven’t been clinically proven as of yet. Most, if not all, of these are well within our control, PsychCentral reported.

1. Get quality sleep.

Older adults need six to eight hours of consistent sleep. During slumber, toxic proteins implicated in Alzheimer’s disease are flushed out. Sleep gives the brain and body time to restore and reboot. During sleep, your brain consolidates new information from the day and files items away into the right “brain cabinets.”

It is imperative to practice sleep hygiene in order to get quality sleep. That means keep your eyes away from screens like TVs, tablets and smartphones. Put cell phones on “do not disturb” so that they don’t ring or vibrate, waking you up. Some researchers recommend buying an alarm clock, and leaving your phone in another room. In today’s busy, high-tech world, it’s crucial we give our minds and bodies adequate rest.

2. Manage your stress levels.

Although there isn’t yet a cure for Alzheimer’s, other medical illnesses or even depression can bring about memory and concentration problems, which if unchecked can lead to dementia. High stress encourages behaviors that increase the risk of dementia. Those behaviors include but are not limited to decreased physical activity, poor eating habits, increased social isolation and self-medication through alcohol or drugs. These factors play a major role in the risk of memory disturbances.

Meanwhile, too much stress and anxiety may lead to physical changes in the brain. For example, high levels of anxiety and chronic stress can usher changes to parts of the brain that handle emotion, thinking and memory, mainly the hippocampus and prefrontal cortex, whereby we process our decision making abilities. The hippocampus, our brains memory center is one of the first places Alzheimer’s attacks. But making a direct link between stress and dementia would be premature, as other factors may also be involved.

3. Connect with others.

Relationships are good for the brain and heart. Research is starting to suggest a link between social interaction and improved brain health. Being social builds connections between neurons.

It’s important to note that socializing, however, doesn’t mean binge watching Netflix with friends. Activities that make your brain work give an added benefit. For example, plan a trip with friends, visit museums with your kids, alternate walking or jogging routes with your workout partner or try something new like learning a second language with a friend. All of these novel activities stimulate parts of the brain that help to retain information, keep it sharp and resilient.

4. Eat a Mediterranean diet.

Healthy eating can delay aging in the brain and body. The Mediterranean diet in particular — plant-based foods such as nuts, legumes, fruit, vegetables, whole grains — is associated with reduced risk of heart disease, cancer, Parkinson’s, Alzheimer’s diseases, as well as other forms of dementia. Fish such as salmon and sardines are high in omega-3 fatty acids — the good fats. In contrast, the fat in red meat is not healthy for your heart or brain.

Healthy eating activates the brain’s metabolic pathways and improves cognitive function. It may slow or prevent Alzheimer’s disease altogether, a notion that many scientists agree on.

5. Exercise

The brain’s processing speed can begin to decline when you’re 25. Exercise bulks up existing neurons, expedites neuronal growth and improves communication between brain cells. While some may find this hard to believe, your actions now can hurt or benefit you later on in life. According to guidelines from the surgeon general, older adults need at least 2.5 hours of moderate-intensity aerobic exercise every week, and two or more days per week of resistance training.

What’s very interesting to note is, for example, recent studies have pointed to older adults who have no Alzheimer’s symptoms despite elevated levels of proteins linked to the disease in their brain. It’s possible that the brains of these individuals were resilient due to lifestyle choices made earlier in life. This may go to show how much of this disease may be environmental, with regards to the life choices we make.

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