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.
The landscape of experimental Alzheimer’s disease (AD) drugs is strewn with failures, so much so that it has been referred to as “an unrelenting disaster zone”. Recognizing the greatly increasing number of patients with this disease, many biopharma companies have invested a lot of resources in attacking this problem, only to be turned away in late stage studies as happened to Merck with its BACE inhibitor, verubecestat, and Lilly with its beta-amyloid antibody, solanezumab.
Now add Biogen to the list of companies that have failed in this arena. Its drug, aducanumab, partnered with Eisai, was believed to be better in removing beta-amyloid from the brain than any agent previously tested. Many have hypothesized that beta-amyloid causes the formation of damaging clumps of debris in the brain leading to AD. Unfortunately, Biogen halted a major clinical trial with aducanumab due to a futility analysis showing that the drug doesn’t work.
This is a terrible result for Alzheimer’s patients who had hoped that this was the drug that would finally succeed in treating AD. But the demise of aducanumab is also disastrous for Biogen which had expended an enormous amount of resources into this program, likely at the expense of other opportunities. It was a risky bet and one for which Wall Street has delivered a punishing blow. Biogen’s stock dropped by nearly 30% shortly after announcing the disappointing aducanumab results.
How is Biogen going to respond? As John Carroll has reported, many industry analysts believe that there aren’t many gems in the Biogen pipeline that can make up for the loss of this potential blockbuster. In predicting Biogen’s next steps, perhaps there are some learnings from another such pipeline failure – that of Pfizer’s torcetrapib.
Torcetrapib was the first of a class of compounds known as CETP inhibitors, drugs that both raised HDL-cholesterol and lowered LDL-cholesterol. A CETP inhibitor had the potential to remodel a heart patient’s lipid profile thereby greatly reducing his risk of a heart attack or stroke. There was tremendous excitement generated in this potential breakthrough treatment, not just in Pfizer but also among cardiologists and heart patients. In fact, internal commercial analyses predicted annual sales in excess of $15 billion. However, as happened with aducanumab, on December 4th, 2006, Pfizer announced that torcetrapib failed its long-term clinical study. The drug was dead. The Wall Street reaction was swift, albeit not as dramatic as Biogen’s experience. Pfizer stock dropped 10% as a result of this news.
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Internally, the Pfizer reaction was intense. Torcetrapib was supposed to be the blockbuster that would drive growth into the next decade. Its loss created an enormous hole. Pfizer CEO Jeff Kindler responded in a couple of ways. First, he decided to “right size” R&D in relation to lower expected future revenues. In effect, hundreds of millions of dollars needed to be cut from R&D. Pfizer’s R&D budget had already undergone major portfolio adjustments and reorganizations over the previous five years due to the acquisition of Warner-Lambert Parke-Davis in 2000 followed by the acquisition of Pharmacia in 2004. Meeting the new R&D budget targets weren’t going to be achieved by simple cuts; rather, major research sites had to be closed and jobs had to be eliminated. Gone were R&D sites around the world including those in France, Japan and, most significantly, the iconic laboratory in Ann Arbor, Michigan.
But budget cuts weren’t going to be enough for Pfizer to meet its desired goals. The company began assessing major M&A opportunities and in 2009 it acquired Wyeth for $68 billion leading to yet another round of reorganizations and portfolio reshuffling. The ripple effect of the torcetrapib demise was felt by the entire company and lasted for a number of years.
So, how will Biogen respond? Undoubtedly, there will be budget cuts. In addition, perhaps Biogen will look at its R&D portfolio and give a higher priority to those programs that have the potential to deliver revenues in the short term. There might also be a push to drop programs deemed to be very risky or where the proof-of-concept requires long, expensive clinical trials. Finally, it wouldn’t be surprising to see Biogen become aggressive in their M&A activities. But make no mistake. The death of an important drug like aducanumab will have both a short and a long term effect on Biogen as a company and especially on R&D.
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……..