
Ozzy Osbourne's Death Puts Spotlight on Rare Form of Parkinson's
'It's been terribly challenging for us all,' Osbourne said in a 2020 Good Morning America interview when he publicly announced his diagnosis.
'There's so many different types of Parkinson's,' Osbourne's wife, Sharon, said during the interview. 'It's not a death sentence by any stretch of the imagination, but it does affect certain nerves in your body.'
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Osbourne's cause of death was not disclosed. The late heavy metal musician had often openly shared his intense lifestyle and experience with drug use, which may have worsened the progression of his form of Parkinson's, according to the New York Times.
What Do We Know About Parkin?
Parkinson's disease is a neurodegenerative condition in which nerve cells, largely in the basal ganglia of the brain, deteriorate or die. According to the National Institutes of Aging, the illness typically progresses with age (most people develop the disease after age 60) and is known for causing tremors, stiff muscles, balance issues, slowed movement and other mobility problems. People may also experience difficulty swallowing, chewing and speaking as well as mental health issues, including depression and mood changes. Emerging research suggests that acting out dreams might also predict Parkinson's disease.
PRKN, which is one of the genes implicated in Parkinson's disease, is involved in maintaining mitochondrial function, which could affect cellular energy—but how that exactly leads to disease is unclear, according to Medline Plus. Parkinson's disease is linked to more than 200 mutations, some of which may cause issues with protein production, durability and function.
In the 2020 Good Morning America interview, the Osbourne family disclosed that he had Parkin 2.[LY1] Osbourne had volunteered to have his genome sequenced in 2010 to see if his DNA could offer more clues about his health and condition.
'He was really curious to know about his Parkinson's-like symptoms, so we looked pretty closely in his genome for that kind of stuff. We found a few hints, but we couldn't tell him why he has symptoms like a tremor. And frankly, his history of drug abuse probably contributed to that, too,' Nathan Pearson, then research director of Cofactor Genomics which sequenced Osbourne's genome, told Scientific American in 2010.
Does Parkinson's Disease Cause Death?
Data on Parkinson's disease and mortality are inconsistent, with some studies suggesting that those with the condition, particularly an advanced or severe form, have about a 1.5 times higher death rate than the general population, according to the American Parkinson Disease Association. Parkinson's disease in combination with another disease or injury, such as a fall, ulcer or pneumonia, could also increase the likelihood of death.
While uncurable, Parkinson's is considered a livable disease. Drugs that act on certain brain neurotransmitters, including dopamine —a hormone involved in movement—can help alleviate symptoms. Research on deep-brain stimulation, which was approved by the U.S. Food and Drug Administration for Parkinson's tremor in 1997, has shown the technology to be a highly effective treatment.
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Newsweek
14 hours ago
- Newsweek
Alzheimer's: Scientists Discover What Sparks Disease
Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. Lithium deficiency in the brain could be a cause of Alzheimer's disease—and a new potential target for treatment. Ten years in the making, this is the finding of researchers at Harvard Medical School who have revealed how lithium plays an essential role in brain function and may provide resistance against brain aging and Alzheimer's. Lithium is a chemical element, currently used as medicine to treat mood disorders like mania and bipolar disorder. "Most people associate lithium with psychiatric treatment. Our study shows, for the first time, that naturally occurring lithium plays a crucial role in maintaining brain health during aging—even at concentrations far below those used in clinical psychiatry," study authors Bruce Yankner and Liviu Aron told Newsweek. The findings are based on a series of experiments in mice and on analyses of human brain tissue and blood samples from individuals in various stages of cognitive health. Lithium carbonate tablet bottles on shelf. Lithium carbonate tablet bottles on shelf. Getty Images "We found that lithium is uniquely depleted in the brains of people with mild cognitive impairment—a precursor to Alzheimer's. This makes lithium deficiency one of the earliest biochemical signs of the disease, possibly years before clinical symptoms appear," the duo explained. "We also saw that higher endogenous lithium levels were associated with preserved cognitive function even in individuals without Alzheimer's. So, this isn't just about preventing disease—it's about supporting healthy brain aging in general. The new revelation helps to explain why some people with Alzheimer's-like abnormalities in the brain don't go on to develop the disease. While genetic and environmental factors play a role, scientists also haven't been able to suggest why some people with the same risk factors might develop it and others don't—until now. The scientists unearthed that lithium loss in the human brain is one of the earliest changes leading to Alzheimer's. In mice, meanwhile, similar lithium depletion accelerated brain pathology (disease or abnormality) and memory decline. They also found reduced lithium levels stemmed from binding to amyloid plaques (misfolded proteins found between nerve cells found in the brains of people with Alzheimer's) and impaired uptake in the brain. One pair of boxes shows fewer green amyloid clusters on the left and more on the right. Another pair of boxes shows a dim arc of purple and red tau on the left and a... One pair of boxes shows fewer green amyloid clusters on the left and more on the right. Another pair of boxes shows a dim arc of purple and red tau on the left and a brighter arc on the right. More Yankner Lab In their final set of experiments, they found a new lithium compound that avoids "capture" by amyloid plaques restored memory in mice. "In people that start experiencing memory loss, the so-called mild cognitive impairment, lithium gets trapped by amyloid plaques—reducing its availability just when it's most needed to protect against inflammation and neurodegeneration," Yankner and Aron explained. "This creates a self-perpetuating feedback loop of worsening pathology and accelerating disease progression and memory loss." This all ties together decades-long observations in patients and provides a new theory of the disease and strategy for early diagnosis, prevention and treatment, according to the researchers. Recently developed treatments that target amyloid beta (a key component of the amyloid plaques) typically don't reverse memory loss and only modestly reduce the rate of decline. "The idea that lithium deficiency could be a cause of Alzheimer's disease is new and suggests a different therapeutic approach," said Yankner in a statement. Researchers had previously found lithium to be the only metal that had markedly different levels across people with and without Alzheimer's at different stages. But Yankner added in a statement, "Lithium turns out to be like other nutrients we get from the environment, such as iron and vitamin C. "It's the first time anyone's shown that lithium exists at a natural level that's biologically meaningful without giving it as a drug." Previous population studies have shown that higher lithium levels in the environment, including in drinking water, tracked with lower rates of dementia. Woman hugging her elderly mother. Woman hugging her elderly mother. PIKSEL/Getty Images Yankner's team demonstrated in mice that lithium depletion isn't just linked to Alzheimer's, it actually helps drive it. This raises hope that one day lithium could be used to treat the disease in its entirety rather than focusing on a single factor like amyloid beta or tau (another Alzheimer's-associated protein), Yankner said. Crucially, the researchers discovered that as amyloid beta begins to form deposits in the early stages of dementia in both humans and mouse models, it binds to lithium, reducing lithium's function in the brain. The reduced levels of lithium affect all major brain cell types and, in mice, lead to changes similar to those seen in Alzheimer's disease, including memory loss. Treating mice with the most potent amyloid-evading compound, called lithium orotate, reversed Alzheimer's pathology, prevented brain cell damage and restored memory. While the findings need to be confirmed in humans through clinical trials, they suggest that measuring lithium levels could help screen for early Alzheimer's. They also highlight the importance of testing amyloid-evading lithium compounds for treatment or prevention. While other lithium compounds are already used to treat bipolar disorder and clinical depression, they are given at much higher concentrations that can be toxic to some people, the researchers flag. Yankner's team discovered lithium orotate is effective at one-thousandth that dose— enough to mimic the natural level of lithium in the brain. Mice treated for nearly their entire adult lives showed no evidence of toxicity, the study found. If further studies confirm these findings, the researchers say lithium screening through routine blood tests may one day offer a way to identify individuals at risk for Alzheimer's who would benefit from treatment to prevent or delay disease onset. "Our study adds to growing evidence that Alzheimer's may be preventable—with something as simple as keeping brain lithium at healthy levels as we age," said Yankner and Aron. "Clinical trials [on humans] could test the impact of low-dose supplementation on cognitive health and dementia risk." Before lithium is proved to be safe and effective in protecting against neurodegeneration in humans, Yankner emphasized that people should not take lithium compounds on their own. Do you have a health story to share with Newsweek? Do you have a question about Alzheimer's? Let us know via health@ Reference Aron, L., Ngian, Z. K., Qiu, C., Choi, J., Liang, M., Drake, D. M., Hamplova, S. E., Lacey, E. K., Roche, P., Yuan, M., Hazaveh, S. S., Lee, E. A., Bennett, D. A., & Yankner, B. A. (2025). Lithium deficiency and the onset of Alzheimer's disease. Nature.


Boston Globe
15 hours ago
- Boston Globe
New hope for Alzheimer's: Groundbreaking Harvard study finds lithium reverses brain aging
The research suggests a new approach to preventing and treating the mind-robbing disease. Advertisement 'It seems to somehow turn back the clock,' said the team's senior author, Dr. The findings come amid a rising tide of Alzheimer's and growing urgency to pinpoint an effective treatment for the For years, researchers believed the buildup of sticky clumps of protein, known as amyloid plaques, fueled the devastating cascade of brain degeneration in Alzheimer's. But Advertisement Yankner now believes that may be a lithium deficiency. Dr. Bruce Yankner sat in his office at Harvard Medical School next to a photograph of a brain with Alzheimers on Monday, Aug. 4. Heather Diehl/For The Boston Globe Lithium has long been used to treat mental health conditions, particularly bi-polar disorder. But the form of lithium typically used for such treatments, lithium carbonate, is different than the one used by the Yankner team, which employed lithium orotate . His team studied brain tissue donated from about 400 people post mortem, as well as blood samples and a battery of memory tests performed yearly before their death. The participants ranged from cognitively healthy at the time of their death to having full-blown Alzheimer's. The scientists found higher levels of lithium in cognitively healthy people. But as amyloid began forming in the early stages of dementia, in both humans and in mice, the amyloid bound to the lithium, restraining it and reducing its availability to surrounding brain cells. That depleted the lithium even in parts of the brain that were amyloid free, essentially reducing lithium's protective function. To test whether lithium depletion was driving the disease or simply a byproduct of it, they fed healthy mice a lithium-restricted diet, draining their lithium levels. This appeared to accelerate their brain aging process, creating inflammation and reducing the ability of nerve cells to communicate. That spurred memory loss in the mice, as measured by their diminished performance in several laboratory memory tests. The researchers then fed a restricted-lithium diet to mice that were genetically engineered to develop Alzheimer's-like amyloid plaques and abnormal tangles of another protein, called tau, and witnessed a dramatic acceleration of the disease. Advertisement These images show what happens to the brains of Alzheimer's mice when they are placed on a lithium deficient diet. It shows that lithium deficiency markedly increases the number of amyloid plaques and the number of tangle-like structures in the brain, resembling advanced Alzheimer's disease in humans. Yankner Lab But they were able to reverse the disease-related damage and restore memory function, even in older mice with advanced disease, by returning lithium to their diet. (Lithium orotate, the compound the scientists used, can evade capture by Alzheimer's amyloid plaques). These images show that treatment of the Alzheimer mice with a very low dose of lithium orotate almost completely abolishes both the plaques and the tangle-like structures. Yankner Lab Other scientists not involved in the research said the findings create a new approach to designing medications to treat and prevent Alzheimer's. 'This study is looking at it from a novel angle,' said 'I didn't expect that the lithium level [in our body] would be this critical,' she said. 'I just hadn't thought about it this way.' The amount of lithium in medications used for mental health conditions is very high and can be toxic to elderly patients. But the amount of lithium used by Yankner's team was one-thousandth the level, essentially mimicking the amount naturally found in the brain. Indeed, mice fed tiny amounts throughout their adult life showed no signs of toxicity. Earlier research has suggested a link between sustained intake of lithium and lower levels of dementia. Notably, Advertisement 'When we're thinking about the therapeutics of a replacement, if you're lowering something, you just have to replace it back to the natural levels,' he said. 'That seems a lot safer than introducing something that our body is not used to, or doesn't already need in order to function. ' 'That's a really good rationale for pursuing it,' he said. A number of factors are linked through research to a higher risk of Alzheimer's and dementia including advanced age, family history, and genetics, as well as several modifiable factors such as diet, smoking, hypertension and diabetes. Liviu Aron, first author of the study that links lithium deficiency to Alzheimer's disease, looked at samples of human and mouse brains in the Harvard lab on Aug. 4. Heather Diehl/For The Boston Globe Many foods already touted for their health benefits naturally contain higher amounts of lithium — But Kaeberlein and other researchers said the real test of the Harvard team's findings would be a large clinical trial in people, with half of the participants receiving small doses of lithium orotate and the others a sham substance, to compare the findings. Kaeberlein said the safety track record of this form of lithium, which showed no toxicity in animals, may help speed trials in people. Advertisement The Harvard findings 'line up with a lot of earlier work, both in the brain and in normal aging,' Kaeberlein said. And he added something rarely heard from scientists when discussing cutting-edge research and a potential medication that may fundamentally change the course of a dreaded disease. This work, he said, 'feeds my optimism that this will lead to potential therapeutics.' But one obstacle to advancing the research is the freeze on Kay Lazar can be reached at


Fox News
18 hours ago
- Fox News
CDC issues China travel warning over chikungunya virus outbreak
The U.S. Centers for Disease Control and Prevention warned Americans to take "enhanced precautions" while traveling to China over an outbreak of the mosquito-borne chikungunya virus. The agency issued a fresh travel warning this month saying that cases of the illness are rapidly spreading in Guangdong province, with most being reported in the city of Foshan. Chinese health officials said more than 7,000 cases have been confirmed there since June 2025. "Most people infected with chikungunya virus develop some symptoms. Symptoms of chikungunya usually begin 3–7 days after a bite by an infected mosquito," according to the CDC. "The most common symptoms are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, or rash. Most people get better within a week; however, some can have severe joint pain for months to years following acute illness." "People at risk for more severe disease include newborns infected around the time of birth, older adults (65 years or older), and people with medical conditions such as diabetes or heart disease. Death from chikungunya is rare," the CDC added. "There is no specific treatment for chikungunya." In Foshan, efforts to combat the virus include drones being sent out to identify mosquito breeding sites, workers spraying residents with mosquito repellent before allowing them into buildings and mosquito-eating fish being released into ponds, the New York Times reported. The European Centre for Disease Prevention and Control said that as of July, there had been around 240,000 global cases of the chikungunya virus across 16 countries and territories. The cases have been linked to 90 deaths. The CDC said in addition to China, there are outbreaks in countries including Bolivia, Kenya and Sri Lanka. Americans traveling to Brazil, Colombia, India, Mexico, Nigeria, Pakistan, the Philippines and Thailand also are at elevated risk of exposure to the virus. "You can protect yourself by preventing mosquito bites, which includes using insect repellent; wearing long-sleeved shirts and pants; and staying in places with air conditioning or that have screens on the windows and doors," the CDC said in its advisory. "Vaccination is recommended for travelers who are visiting an area with a chikungunya outbreak," the CDC continued, noting that there are currently two approved chikungunya vaccines in the U.S. "Seek medical care immediately if you develop fever, joint pain, headache, muscle pain, joint swelling, or rash during or after travel," the CDC advised.