The brain of a sleep-deprived person is imbued with excess of two proteins that are substantially associated with Alzheimer’s disease.
According to the study published in the journal Science, a protein called tau is found in excess in the fluid that fills the brain and spinal cord of individuals with chronic sleep deprivation. The protein also drives neuron degeneration, and during Alzheimer’s, it scatters throughout the brain.
Similarly, sleep deprivation also induces accumulation of protein called amyloid-beta – a chunk of which dots the brains of Alzheimer’s patients.
In the study, researchers went over the samples of cerebrospinal fluid of eight adult participants who were sleep-deprived for nearly 36 hours. They found 51.5 percent increase in their tau levels. Similarly, mice that were rob of sleep were found to have twice the level of tau compared to well-rested ones.
Another study also reported that the lack of sleep to be the legitimate cause of increased level of A-beta in the cerebrospinal fluid, and if preceded by a week of poor sleep, the levels of tau also increased.
Since lack of sleep increases the levels of tau and A-beta in the brain, it appears that the only way to curtail the risk of developing Alzheimer’s symptom is to treat sleep disorders during mid-life and get good amount of sleep as much as possible. Proper sleep helps our brain get rid of excess proteins and other unnecessary stuffs, so getting less sleep means that wash cycle is disturbed.
Lack of sleep is tied to increases in two Alzheimer’s proteins (Science News)
The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans (Science)
Association of Excessive Daytime Sleepiness With Longitudinal β-Amyloid Accumulation in Elderly Persons Without Dementia (Jama Neurology)
This 4-minute video shows how Alzheimer’s disease changes the brain and looks at promising ideas to treat and prevent the disease. Alzheimer’s disease is the most basic form of dementia, and scientists are trying to understand how the affects the nervous system. This video illustrates how neurons communicate in a healthy brain compared to that of a person with Alzheimer’s disease. In a healthy brain, cells such as astrocytes and microglia help keep neurons healthy by clearing away debris that builds up over time. In a person with Alzheimer’s disease, toxic changes in the brain destroy the ability of these cells to maintain a healthy environment for the neurons in the brain, ultimately causing a loss of neurons. Researchers believe that the Alzheimer’s disease process involves two proteins: beta amyloid protein and tau protein. Within the brain of a person with Alzheimer’s disease, these proteins become compromised. Over time, abnormal tau accumulates and eventually forms tangles inside the neurons, and the beta amyloid clumps into plaques, which build up between the neurons. As the level of amyloid increases, tau rapidly spreads throughout the brain. Other changes that affect the brain may play a role in the disease, such as the inability of the vascular system to deliver enough blood and nutrients to the brain. These factors cause the brain to shrink in size, starting with the hippocampus. A person with Alzheimer’s gradually loses the ability to think, remember, make decisions, and function independently. Researchers are working on the key to understanding Alzheimer’s disease so that Alzheimer’s disease research can lead to the development of more effective therapies with the hope that we can delay or even prevent the devastation of dementia. This video was developed by the National Institute on Aging (https://www.nia.nih.gov/), part of the National Institutes of Health (https://www.nih.gov/). Want to learn more? Subscribe to the National Institute on Aging’s YouTube channel: https://www.youtube.com/user/NatlInst…. Find more information about Alzheimer’s disease from the National Institute on Aging: https://www.nia.nih.gov/health/alzhei…. Find more health information from the National
People who donate their bodies to science might never have dreamed what information lies deep within their brains.
Even when that information has to do with sleep.
Scientists used to believe that people who napped a lot were at risk for developing Alzheimer’s disease. But Lea Grinberg with the UCSF Memory and Aging Center started to wonder if “risk” was too light a term — what if, instead, napping indicated an early stage of Alzheimer’s?
About a decade ago, Grinberg — a neuropathologist and associate professor — was working with her team to map a protein called tau in donated brains. Some of their data, published last week, revealed drastic differences between healthy brains and those from Alzheimer’s patients in the parts of the brain responsible for wakefulness.
Wakefulness centers in the brain showed the buildup of tau — a protein that clogs neurons, Grinberg says, and lets debris accumulate. Gradually, these clogged neurons die. Some areas of the diseased brains had lost as much as 75% of their neurons. That may have led to the excessive napping scientists had observed before. Although the team only studied brains from 13 Alzheimer’s patients and 7 healthy individuals, Grinberg says that the degeneration caused by Alzheimer’s was so profound they were sure of its significance.
“We are kind of changing our understanding of what Alzheimer’s disease is,” she says. “It’s not only a memory problem, but it’s a problem in the brain that causes many other symptoms.”
Although these symptoms aren’t as severe as complete loss of memory or motor functions, Grinberg says they can still hold real consequences for a person’s quality of life. “Because if you don’t sleep well every day and if you… are not in the mood to do things like you were before, it’s very disappointing, right? My grandparents were like this.”
Grinberg says it’s important to know whether napping could be an early sign of Alzheimer’s, for treating symptoms and developing drugs that could slow the progression of the disease. Although there are no prescription drugs available to treat tau buildup, she says, a few are in clinical trials.
A public health professor and neuroscientist at UC Berkeley says the new information offers hope to researchers. William Jagust, who has studied Alzheimer’s for over 30 years, says the results could help select patients for clinical trials of new drugs that require early treatment. “It’s also just very important for understanding the evolution of Alzheimer’s disease with the hope that we eventually will have a drug,” he adds.
It’ll be awhile before doctors can diagnose anyone with Alzheimer’s based on how often they doze off. “There’s no practical application of this to clinical medicine as of today,” Jagust says, “but I think it’s on the cutting edge of the very, very important questions.”
What is Alzheimer’s disease? Alzeimer’s (Alzheimer) disease is a neurodegenerative disease that leads to symptoms of dementia. Progression of Alzheimer’s disease is thought to involve an accumulation of beta-amyloid plaque and neurofibrillary tangles in the brain. Find more videos at http://osms.it/more. Study better with Osmosis Prime. Retain more of what you’re learning, gain a deeper understanding of key concepts, and feel more prepared for your courses and exams. Sign up for a free trial at http://osms.it/more. Subscribe to our Youtube channel at http://osms.it/subscribe. Get early access to our upcoming video releases, practice questions, giveaways and more when you follow us on social: Facebook: http://osms.it/facebook Twitter: http://osms.it/twitter Instagram: http://osms.it/instagram Osmosis’s Vision: Empowering the world’s caregivers with the best learning experience possible.
More and more studies are showing how regular exercise benefits the brain, and in particular, the aging brain. What’s less clear is how exactly exercise counters the cognitive decline that comes with aging and diseases like Alzheimer’s.
To find out, for nearly a decade, Ozioma Okonkwo, assistant professor of medicine at the University of Wisconsin School of Medicine and Public Health and his colleagues have studied a unique group of middle-aged people at higher risk of developing Alzheimer’s. Through a series of studies, the team has been building knowledge about which biological processes seem to change with exercise.
Okonkwo’s latest findings show that improvements in aerobic fitness mitigated one of the physiological brain changes associated with Alzheimer’s: the slowing down of how neurons breakdown glucose. The research, which has not been published yet, was presented at the annual meeting of the American Psychological Association on Aug. 9.
Okonkwo works with the 1,500 people on the Wisconsin Registry for Alzheimer’s Prevention (WRAP)—all of whom are cognitively normal, but have genes that put them at higher risk of developing Alzheimer’s, or have one or two parents who have been diagnosed with the disease, or both. In the latest study, Okonkwo recruited 23 people from the WRAP population who were not physically active. Eleven were asked to participate in an exercise regimen to improve their aerobic fitness for six months, and 12 served as the control.
All had their brains scanned to track Alzheimer’s-related brain changes including differences in how neurons metabolized glucose, since in people with Alzheimer’s glucose breakdown slows. At the end of the study period, the group that exercised more showed higher levels of glucose metabolism and performed better on cognitive-function tests compared to the controls.
“We are carrying our research full circle and beginning to demonstrate some causality,” says Okonkwo about the significance of his findings.
In their previous work, he and his team identified a series of Alzheimer’s-related biological changes that seemed to be affected by exercise by comparing, retrospectively, people who were more physically active to those who were not.
In this study, they showed that intervening with an exercise regimen could actually affect these processes. Taken together, his body of research is establishing exactly how physical activity contributes to significant changes in the biological processes that drive Alzheimer’s, and may even reduce the effect of strong risk factors such as age and genes linked to higher risk of neurodegenerative disease.
For example, in their earlier work his group confirmed that as people age, the presence of Alzheimer’s-related brain changes increases—including the buildup of amyloid, slower breakdown of glucose by brain cells, shrinking of the volume of the hippocampus (central to memory), and declines in cognitive function measured in standard recall and recognition tests.
But they found that in people who reported exercising at moderate intensity at least 150 minutes a week, as public health experts recommend, brain scans showed that these changes were significantly reduced and in some cases non-existent compared to people who were not active. “The association between age and Alzheimer’s brain changes was blunted,” says Okonkwo, “Even if [Alzheimer’s] got worse, it didn’t get worse at the same speed or rate among those who are physically active as in those who are inactive.”
In another previous study, they found the benefits of exercise in controlling Alzheimer’s processes even among those with genetic predisposition for the disease. When they divided the participants by fitness levels, based on a treadmill test and their ability to efficiently take in oxygen, they found that being fit nearly negated the effect of the deleterious gene ApoE4. “It’s a remarkable finding because it’s not something that was predicted,” says Okonkwo.
In yet another previous study, Okonkwo and his team also found that people with higher aerobic fitness showed lower amounts of white matter hyperintensities, brain changes that are signs of neuron degeneration and show up as brighter spots on MRI images (hence the name). White matter hyperintensities tend to increase in the brain with age, and are more common in people with dementia or cognitive impairment.
They form as neurons degrade and the myelin that surrounds their long-reaching arms—which helps nerves communicate with each other effectively—starts to deteriorate. In people with dementia, that process happens faster than normal, leading to an increase in white matter hyperintensities. Okonwko found that people who were more aerobically fit showed lower amounts of these hyperintensities than people who were less fit.
Given the encouraging results from his latest study of 23 people that showed intervening with exercise can change some of the Alzheimer’s-related brain changes of the disease, he plans to expand his small study to confirm the positive effect that exercise and better fitness can have in slowing the signs of Alzheimer’s. Already, his work has inspired a study launched earlier this year and funded by the National Institutes of Health that includes brain scans to track how physical activity affects biological factors like amyloid and glucose in people at higher risk of developing Alzheimer’s.
The cumulative results show that “there may be certain things we are born with, and certain things that we can’t change ]when it comes to Alzheimer’s risk], but a behavior like physical exercise might help us to modify that,” says Heather Snyder, vice president of medical and scientific relations at the Alzheimer’s Association.
A realization came to me in mid-December. Someone I was close to, had spoken to almost every day for a year and a half, began ignoring me. It was easy to notice. I stepped away from all social media not wanting to be reminded that I’m being ignored. Maybe I said something that bothered this […]
Robert Moir was damned if he did and damned if he didn’t. The Massachusetts General Hospital neurobiologist had applied for government funding for his Alzheimer’s disease research and received wildly disparate comments from the scientists tapped to assess his proposal’s merits. It was an “unorthodox hypothesis” that might “fill flagrant knowledge gaps,” wrote one reviewer, but another said the planned work might add little “to what is currently known……..
More than 30 million people worldwide suffer from Alzheimer’s disease – the most common form of dementia. Unfortunately, there is no cure, only drugs to ease the symptoms. However, my own research suggests a way to treat the disease. I have found the strongest evidence yet that the herpes virus is a cause of Alzheimer’s, suggesting that effective and safe antiviral drugs might be able to treat the disease. We might even be able to vaccinate our children against it……..
Working with the Brazilian Biobank for Aging Studies (BBAS) at the University of São Paulo, investigators at the University of California in San Francisco (UCSF) studied results of postmortem brain tissue tests and compared them with psychiatric symptoms obtained from detailed interviews conducted with people who knew the deceased well, such as relatives and carers. They suggest that their study — a paper on which now features in the Journal of Alzheimer’s Disease — reveals that psychiatric symptoms are not the cause of Alzheimer’s, but more likely early indicators of the disease…….
Alzheimer’s disease (AD) is the most common form of dementia. It takes a devastating toll on patients and family members, who are usually the caregivers. Current drugs only treat symptoms of AD, not its causes.
FIU researchers are studying a new approach to treating Alzheimer’s using nanotechnology aimed at reducing the inflammation in the brain.
“Current drugs affect neuro-transmitters in the brain. However, inflammation is still clearly present in patients with AD—and seems to be a root cause,” says Madhavan Nair, associate dean for biomedical research and vice president for nanotechnology at Herbert Wertheim College of Medicine.
According to the Alzheimer’s Association, more than 5 million Americans are living with Alzheimer’s; someone in the U.S. develops the disease every 66 seconds; and it is the 6th leading cause of death in the United States – killing more people than breast cancer and prostate cancer combined. June is Alzheimer’s and Brain Awareness Month.
Nair and his team will target brain cells called microglia and will use his FIU patented MENs (magneto electric nanoparticles) carrier system for the specific delivery and sustained release of two
anti-inflammatory drugs, Withaferin A and CRID3, into those cells.
“We are hoping that this will inhibit the neuroinflammatory response in microglia and thus help to improve cognitive function in AD patients,” Nair says. The study is funded by a $224,643 grant from the Florida Department of Health.
Although scientists are not sure what causes cell death and tissue loss in the Alzheimer’s brain, they suspect plaques and tangles are to blame. The plaques form when protein pieces called beta-amyloid clump together between nerve cells (neurons) in the brain.
Investigators in Nair’s lab are using sophisticated technology –bioinformatic tools and 3D structure of beta-amyloid – to find the binding site of these anti-inflammatory drugs on beta-amyloid. These studies could translate into new therapies in the treatment of Alzheimer’s.
If everyone who read the articles and like it, that would be favorable to have your donations – Thank you.