Latest news with #dopamine
Health Line
3 days ago
- Health
- Health Line
Types of Parkinson's
Key takeaways Parkinson's disease is often caused by the death of cells in the brain that produce dopamine, leading to symptoms like tremors and difficulty with balance and movement. Besides the most common form, idiopathic Parkinson's, there are various other types, including juvenile Parkinson's, drug-induced parkinsonism, and vascular parkinsonism, each with distinct causes and characteristics. Diagnosing Parkinson's involves a review of symptoms, medical history, and neurological tests, and while there's no single test, blood tests, genetic testing, DaTscans, and MRIs can help rule out other conditions. Parkinson's disease is a neurological condition that gets progressively worse over time and causes trouble with movement. It's thought to affect about 1 percent of people over the age of 65. Parkinson's is caused by the death of cells in a part of your brain called the substantia nigra. When these cells die, levels of the neurotransmitter dopamine drop in your brain. This reduction leads to symptoms such as tremors, impaired balance, rigid muscles, and difficulty walking. Collectively these symptoms are known as parkinsonism. Parkinson's disease is attributed to about 85 percent of parkinsonism cases. The other 15 percent of cases are attributed to one of several conditions called atypical parkinsonisms. Learn about the different types of Parkinson's and how they're diagnosed. Idiopathic Parkinson's disease Idiopathic Parkinson's, or simply Parkinson's disease, is the most common cause of parkinsonism. It generally onsets between the ages of 55 to 65 and rarely occurs before the age of 50. Parkinson's onsets gradually as cells in the substantia nigra die and dopamine levels drop. It's thought genetic and environmental factors contribute to the development of Parkinson's. The main symptoms of Parkinson's disease include: Juvenile and young-onset Parkinson's disease Juvenile Parkinson's is a rare condition that onsets before the age of 21. It's referred to as young-onset Parkinson's if it presents before the age of 40. Symptoms are similar to late-onset Parkinson's, but it's more likely to be associated with genetic causes than late-onset Parkinson's. A 2017 study of 108 people with early-onset Parkinson's found that 46.3 percent reported a family history. Drug-induced parkinsonism Drug-induced parkinsonism is the second most common cause of parkinsonism. It occurs when a drug interferes with dopamine transmission in your body. You become more likely to develop drug-induced parkinsonism with age. In a study published in Movement Disorders, researchers found the average age of onset of drug-induced parkinsonism was 70.9. Symptoms are similar to those of Parkinson's disease, including: tremor rigidity slowness of movement gait disturbance Drugs that can lead to drug-induced parkinsonism include: antipsychotics antidepressants calcium channel antagonists gastrointestinal prokinetics antiepileptic drugs Multiple system atrophy Multiple system atrophy is a rare disorder that causes similar symptoms as Parkinson's such as impaired movement, stiff muscles, and poor balance. It most often onsets in your mid-50s. It can lead to changes in areas such as your: heart rate digestion blood pressure bladder control Progressive supranuclear palsy Progressive supranuclear palsy causes problems with balance, walking, swallowing, eye movement, speech, and mental ability. For most people, it onsets in their mid-60s and it tends to progress more rapidly than Parkinson's disease. The exact cause isn't known, but symptoms are caused by a deterioration of cells in your brain stem, substantia nigra, and other parts of your brain. Corticobasal syndrome Corticobasal syndrome is caused by a buildup of a type of protein called tau in your brain. Symptoms vary but can include: trouble controlling a limb on one side of your body muscle stiffness tremors jerky movement spasms slow or slurred speech symptoms of dementia trouble swallowing It usually onsets between the ages of 50 to 70. Dementia with Lewy bodies Dementia with Lewy bodies is a progressive condition associated with an abnormal buildup of a protein called Lewy bodies, or alpha-synuclein, in your brain. It typically onsets after the age of 50 and affects men slightly more often than women. Dementia with Lewy bodies also has the same movement symptoms of Parkinson's, as well as mental symptoms such as: changes in alertness or concentration hallucinations rapid eye movement sleep disorder memory problems trouble processing information or planning Vascular parkinsonism Vascular parkinsonism is thought to be caused by multiple small strokes in the area of your brain that control movement. It can lead to similar symptoms as Parkinson's but tends to mostly affect the lower body. postural instability mostly lower-body parkinsonism shuffling or freezing gait when walking absence of a resting tremor poor response to medication levodopa Because your risk of having a stroke increases with age, your chance of developing vascular parkinsonism is also thought to increase as you get older. Normal pressure hydrocephalus Normal pressure hydrocephalus is a buildup of cerebrospinal fluid in the cavities in your brain. This buildup can put pressure on your brain and cause damage that leads to parkinsonism. Hydrocephalus is most common in adults over 65. The average age of onset is approximately 70 years. About 80 to 95 percent of people experience gait disturbances described as shuffling, magnetic, or a wide-based gait. About 80 to 95 percent of people also experience cognitive changes such as reduced attention, forgetfulness, or poor executive function. About 50 to 75 percent of people experience loss of bladder control. How is each type diagnosed? A doctor trained in neurogenerative conditions diagnoses Parkinson's based on your symptoms, medical history, and results from a physical and neurological test. No single test can diagnosis Parkinson's disease, but tests may be able to rule out other causes of parkinsonism. These tests include: Blood test. Blood tests can't identify Parkinson's disease directly, but they may be able to help your doctor identify other causes of parkinsonism, such as multiple system atrophy or corticobasal degeneration. Genetic testing. Genetic testing may help your doctor identify the underlying cause of your parkinsonism if you have a family history of parkinsonism. DaTscan. A DaTscan is an imagining technique that lets a doctor see how much dopamine is in your brain. If the scan finds an abnormally low amount, it can help confirm your doctor's Parkinson's diagnosis. Magnetic resonance imagining (MRI). An MRI can potentially identify a brain tumor, normal pressure hydrocephalus, or vascular parkinsonism. Takeaway Parkinson's disease and most other causes of parkinsonism have no known cure. But researchers are continuing to learn more about these conditions and how to best control symptoms.
Medical News Today
3 days ago
- Health
- Medical News Today
New weekly injection may eliminate need for daily pills in Parkinson's
Parkinson's symptoms develop slowly, most commonly after the age of 50, and include tremor, slowness in movement, limb stiffness, problems with gait and balance, sleep disorders, and mental health with Parkinson's disease have to take several tablets each day to help alleviate their a team of scientists in Australia has developed a weekly injectable treatment for Parkinson's further research proves the injection's safety and efficacy, the long-acting implant could be life changing for people living with Parkinson' disease is the second most common neurodegenerative condition after Alzheimer's Disease. It affects almost 1.1 million people in the United States and more than 10 million worldwide. Of these, 96% are diagnosed after the age of condition occurs when nerve cells in an area of the brain called the substantia nigra stop producing enough of the neurotransmitter dopamine. This leads to a range of symptoms, including:Tremor, or shaking, in hands, arms, legs, jaw, or headMuscle stiffnessSlowness of movementImpaired balance and two main treatments for Parkinson's disease are levodopa (L-dopa), which nerve cells use to make dopamine, and carbidopa, which increases the efficacy of levodopa and helps minimize its side effects. However, people need to take the medications several times a day, which many find difficult to scientists in Australia have developed a long-acting injectable treatment combining the two medications. Because the implant releases the drugs slowly over seven days, people with the condition would no longer have to take multiple tablets every study findings suggest that the injection could be 'a promising system for the delivery of levodopa and carbidopa for Parkinson's patients'.Sneha Mantri, MD MS, Chief Medical Officer for the Parkinson's Foundation, who was not involved in the study, agreed:'If this medication is safe and effective in humans, it could be an alternative for people with [Parkinson's] compared to multiple daily pills.'The findings are published in the journal Drug Delivery and Translational alternative to multiple daily pillsThe injection contains a combination of levodopa (L-dopa) and carbidopa, two drugs used together to treat Parkinson's disease. L-dopa can cross the blood-brain barrier into the central nervous system, where it is converted to dopamine. People with Parkinson's take L-dopa to control the physical symptoms associated with the lack of dopamine prescribe carbidopa in combination with L-dopa to increase its efficacy within the nervous system, and help combat gastrointestinal symptoms, which are a common side effect of two drugs are usually taken in the form of capsules, containing a combination of the drugs in carefully calculated proportions. To reduce the chance of gastrointestinal symptoms, they should be taken with meals. As fat and protein can decrease the absorption of L-dopa, people must avoid high fat or high protein meals when taking the was the injection developed, and how does it work?The newly developed injection also administers a combination of L-dopa and carbidopa in the form of an in-situ their implant, the researchers used two organic polymers and a solvent, in different ratios to achieve the correct rate of drug release. Once the correct ratio was determined, levodopa and carbidopa were added to create the performed several in-vitro tests to determine the effect of pH (acid/alkali balance), how easy it was to inject the implant, how rapidly the implant degraded and the drugs were dispersed, and the effect of the implant on then tested the mechanism ex vivo in leg muscle tissue from a implant performed similarly in vitro and ex vivo, releasing the drugs slowly over several injection into muscle tissue, pores formed on the surface of the implant, through which the drugs diffused into the tissue. Up to 90% of the drug was released over 7 days, and the implant broke down completely within 2 formula that the researchers developed was easy to inject, so they suggest that this could be a:'Promising drug delivery system for Parkinson's patients, which will reduce the dosing frequency in the elderly patients to once-a-week injection.'Potential problems with long-acting injectionsJamie Adams, MD, associate professor of Neurology at the University of Rochester Medical Center, who was not involved in the study, highlighted potential problems with the treatment:'Given fluctuations in Parkinson's symptoms, it may be difficult to determine appropriate dosing for an entire week, and patients may still require oral medications or other therapies. If the weekly injection is dosed too high, that could also be problematic.'And Mantri also raised some issues that will need to be addressed:'Every medication is different, and this type of gel has not been used for [Parkinson's] treatment before. However, many injectable medications carry the risk of injection site reactions (for instance, rash, nodules) related to the delivery method itself.'Promising early development needs further testingThis is an early stage of development of a new mechanism of drug delivery for people with Parkinson's disease. But it has the potential to transform treatment for elderly people with Parkinson' there are several further stages of testing that would need to be undertaken before the implant could be licensed, as Mantri told Medical News Today:'This is a very preliminary study, looking at how the new treatment behaves in the lab. Further testing on animals and then humans will be necessary as it moves forward in drug development.''I would like to see the results of animal testing, as well as human testing, to ensure that this is both safe and effective,' she agreed:'This treatment is still early, and there needs to be human studies, including randomized controlled trials, evaluating safety and efficacy.''A weekly injectable therapy for Parkinson's disease could reduce the burden of frequent medication dosing and may improve quality of life.'— Jamie Adams
Medscape
4 days ago
- Health
- Medscape
Watching Peers Eat Can Trigger Overeating, Says Mouse Study
TOPLINE: Even in the absence of hunger, mice increased their sucrose diet intake after observing their peers eat. This effect was abolished by the inhibition of dopamine receptors. METHODOLOGY: Previous studies in humans have shown a significant association between external eating behaviors and watching eating shows, but this has not been confirmed in a mouse model. This study examined whether satiated mice, despite not being hungry, increased their food intake when watching a peer engage in binge-like eating behavior. A total of 14 male mice were divided into two groups: One group was either fed or fasted overnight before testing, and the other group was always fed before testing. Mice were paired according to genetic and parental information and placed in separate but adjacent chambers for interaction without physical contact. Food intake was recorded hourly for 4 hours across different days, using chow, high-fat, and sucrose diets. In a follow-up experiment, the group of mice that was always fed before testing received intraperitoneal injections of saline, a D1 dopamine receptor inhibitor, or a D2 dopamine receptor inhibitor prior to testing. TAKEAWAY: Satiated mice increased their sucrose diet intake during the first hour while watching peers that had fasted eat, with significant increases noted in both the initial and repeated tests (P = .0043 and P = .0154, respectively). No significant increase in chow or high-fat diet intake was observed when satiated mice watched peers that had fasted consume the diets. The increase in sucrose intake persisted after saline injection (P = .0057) but was abolished after the administration of the D1 or D2 dopamine receptor inhibitors. IN PRACTICE: 'Establishing this animal model provides a foundation for future studies on the neurobiological mechanisms underlying cognitive-driven food intake and may contribute to the development of targeted therapeutic strategies for obesity,' the authors of the study wrote. 'This animal model opens the door to developing new treatments that target the brain's reward system to help prevent or reduce overeating,' Yong Xu, PhD, MD, professor and associate director for Basic Sciences at the Children's Nutrition Research Center, Baylor College of Medicine, Houston, said in a news release. 'It also supports public health efforts that aim to limit the influence of visual food cues in media and social settings, which could help people better manage their weight and eating habits.' SOURCE: The study was led by Xu Xu, MD, Baylor College of Medicine, Texas Children's Hospital, Houston. It was presented on June 14, 2025, at the ENDO 2025: The Endocrine Society Annual Meeting in San Francisco. LIMITATIONS: No limitations were discussed in the abstract. DISCLOSURES: No disclosures or conflict of interest statements were provided. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Yahoo
6 days ago
- Health
- Yahoo
How to Start Working Out in the Morning—Even If You're Not a Morning Person
Just as the best type of exercise is the one that you actually enjoy doing, ultimately, the best time to exercise—whether that's afternoon, evening, or morning—is whenever works best with your schedule and lifestyle. Because let's be honest, figuring out how to start working out is hard enough without having to rework your entire routine. That said, if you've been wondering if there's one time of day that's best for exercising, there are some undeniable pros of working out in the morning. Surveys show that you're more likely to stick with a morning workout or exercise program than one later in the day, when you'll likely be distracted by other responsibilities or have time to come up with excuses to skip your fitness session. Research has also found that exercise can help improve mood and sense of well-being by increasing feel-good neurotransmitters like endorphins, epinephrine, norepinephrine, and dopamine. Physical activity also been shown to boost cognitive functioning like memory, attention, concentration, and learning. Needless to say, a sweat session is a great way to begin each day, especially before work or school when you want to be in top mental form. Morning workouts can also help you beat the heat of summer. And if you're participating in any type of fitness event, start times are almost always in the morning. If you want to compete at your optimal level, it's wise to get used to morning workouts. So how do you start working out in the morning without dreading it? Experts have their favorite tips for turning the morning into your preferred time of day to move. Read up and get ready to set your alarm for a few hours earlier than usual. This should be a no-brainer, but if you don't log the sleep you need, you're not going to feel like getting up in the morning, let alone tackling a morning workout. While you should shoot for seven to eight hours of sleep every night, making the switch overnight isn't easy. That's why Jonathan Jordan, a NASM certified personal trainer personal trainer and nutrition coach in San Francisco, tells his clients to add just 30 minutes at a time to their bedtime routine. So if you're usually in bed around 11 p.m., start making a conscious effort to get in bed at 10:30. "Even if you lie quietly in bed and do a little deep breathing or meditation until you fall asleep, it can help," he says. It's not just the amount of sleep you get that matters—sleep quality is important too. One rule Jordan employs with his clients: Adopt a 30- to 60-minute device blackout period before bed. During this time, abandon your use of phones, computers, and light-emitting devices. "Clients who do this [tend to] sleep better, have more energy, and report less stress, better diet, and even better digestion," he says. Also helpful for ensuring deep, uninterrupted sleep is to make your sleep environment as cool, dark, and quiet as possible. Temperature, ambient light, and ambient noise are all environmental factors that can disrupt a sound night's sleep—but that you do have some control over. How appealing does it sound to wake up (at least) an hour earlier just to work hard? Probably not much. So start small. Could you wake up 15 minutes earlier and squeeze in a quick workout (like this 15-minute stairs workout) or a round of full-body stretches? Probably. Get used to doing this for a week or two before moving your wake-up time up another 15 minutes. Repeat until you're up with enough time to log the exercise you want. Progressing slowly will help you adapt to that earlier wake-up call, says Jennie Gall, former owner of Relevé Pilates Studio in Ripon, Calif. Set out your workout clothes, sneakers, gym bag, and whatever else you need for your morning workout the night before. This is the best way to give your future self a helping hand, save some time in the morning, and avoid forgetting anything—especially if you're a little foggy when you wake up. Leaving your alarm clock next to your bed makes it all too easy to hit the snooze button. But if you place it across the room, you'll be forced to get up to turn it off. The extra benefit of doing this if your smartphone is your alarm is that keeps you far away from your phone all night. You'll sleep better. Permission granted to sip that cup of coffee or tea before exercising. Keep your serving to one 8-ounce cup and avoid tons of add-ins like cane sugar and artificial sweeteners. "In moderation, caffeine is widely recognized and safe for sipping pre-workout," Jordan says. In fact, research even suggests that caffeine can aid fitness performance. Read the original article on Real Simple
WIRED
10-07-2025
- Health
- WIRED
Scientists Succeed in Reversing Parkinson's Symptoms in Mice
Jul 10, 2025 6:30 AM The findings of two recent studies give hope that the disease could one day be reversed in humans—but experts warn that this complex disease will likely need multiple complementary treatments. An illustration of the human brain showing a shrunken substantia nigra, a degeneration that occurs with Parkinson's disease. Illustration: KATERYNA KON/SCIENCEAll products featured on WIRED are independently selected by our editors. However, we may receive compensation from retailers and/or from purchases of products through these links. Cases of Parkinson's disease have doubled in the last 25 years, according to figures from the World Health Organization. For decades, the scientists have investigated what triggers this disorder to mitigate its symptoms and anticipate its onset. Now, a series of experimental therapies are laying the groundwork for potentially reversing the condition, which affects nearly 10 million people worldwide and can generate costs of approximately $10,000 per patient per year, when considering direct and indirect medical expenses. Parkinson's disease is a degenerative neurological disorder in which cells that produce dopamine in the brain die, causing symptoms such as tremors, muscle stiffness, slowness of movement, and alterations in balance. So far there is no cure, and treatments are limited. Kay Double, a professor at the University of Sydney's School of Medical Sciences, has been researching the biological mechanisms underlying this disease for more than a decade, with the aim of finding ways to slow or even halt its progression. In 2017, he led a study that identified for the first time an abnormal form of a protein called SOD1 in Parkinson's patients. Under normal conditions, this protein acts as an antioxidant enzyme, protecting brain cells from damage caused by free radicals, highly reactive molecules that contain oxygen and can deteriorate cells if not properly neutralized. Free radicals are produced by natural bodily processes as well as by external factors, like diet, smoking, and exposure to pollution. In people with Parkinson's disease, SOD1 suffers alterations that prevent it from fulfilling its protective function, with it instead accumulating in the brain and causing neuronal damage, according to the findings of Double's team. Based on these results, the team then conducted further research, with results suggesting that copper supplementation in the brain could be an effective way to slow and even reverse the symptoms of Parkinson's (copper is crucial to SOD1's function). To test this hypothesis, they evaluated the efficacy of a drug called CuATSM, designed to cross the blood-brain barrier and deliver copper directly to brain tissue. This experiment, written up and published in Acta Neuropathologica Communications, was divided into two phases. The first was to determine the optimal dose of the drug to induce a response in the brain. To find this, CuATSM was administered daily for three weeks to 27 eight-week-old wild-type mice, with concentrations of copper and other metals then measured in the mice's tissues. This revealed that 15 milligrams per kilogram was the ideal dose to effectively increase the levels of copper in the brain. In the second stage, this dose was applied to 10 mice genetically modified to develop Parkinson's-like symptoms. The animals were divided into two groups: one received CuATSM daily for three months, while the other received a placebo without the active ingredient. The results showed that the mice treated with the placebo experienced a deterioration in their motor skills. In contrast, those that received the copper supplement showed no alterations in their movement. It appears the treatment corrected the dysfunctions of SOD1 and restored its protective properties. In the mice receiving the copper treatment, dopamine neurons were preserved in an area of the brain called the substantia nigra, an area essential for the control of movement, coordination, learning, and certain cognitive functions. 'All of the mice we treated showed dramatic improvement in their motor skills. The results exceeded our expectations and suggest that, after further study, this therapeutic approach could slow the progression of Parkinson's in humans,' says Double. But experts caution that Parkinson's is a complex condition that will likely require multiple combined interventions. A single treatment may have limited effect, but its efficacy may be enhanced by integrating it with other therapeutic approaches. In that context, Double's team's findings could be complemented by recent research from Stanford University focused on restoring communication between neurons in a subtype of Parkinson's linked to mutations in the gene responsible for producing an enzyme called LRRK2. In these cases, the mutation causes hyperactivity of the enzyme, altering the structure of brain cells and disrupting signaling between dopaminergic neurons and those in the striatum, a deep brain region related to movement, motivation, and decision-making. It is estimated that about 25 percent of Parkinson's cases are genetic in origin, and the LRRK2 mutation is one of the most frequent. The team led by Stanford neuroscientist Suzanne Pfeffer proposed that inhibiting the excessive activity of this enzyme could stabilize symptoms, especially if detected in early stages. The goal was to regenerate primary cilia, antenna-like structures that enable communication between cells. The hypothesis was tested in mice genetically modified to exhibit LRRK2 hyperactivity and early symptoms of the disorder. For two weeks, these animals were administered with a compound called MLi-2, which binds to the enzyme and reduces its activity. In this first test, no relevant changes were observed, which the researchers attributed to the fact that the examined neurons and glia—another type of cell in the nervous system, which support neurons—were already mature and were not in the cell division phase. However, a review of the scientific literature revealed that, even if mature, certain neurons can regenerate their primary cilia depending on their sleep-wake cycles. 'The findings that other nonproliferative cells can develop cilia made us think that the inhibitor still had therapeutic potential,' Pfeffer explains. The team then decided to extend the treatment to three months. After this period, they found that the percentage of neurons and glial cells in the striatum with primary cilia was comparable to that of healthy mice without the genetic mutation. This restoration of cellular structures made it possible to reactivate communication between dopaminergic neurons and the striatum. As a result, neurotransmitters affected by the LRRK2 protein induced the production of neuroprotective factors at levels similar to those of a healthy brain, something that had been diminished as a result of LRRK2 hyperactivity. In addition, density markers of dopaminergic nerve endings were doubled, suggesting a possible recovery of previously damaged neurons. 'These findings suggest that it is not only possible to stabilize the disease, but also to improve the condition of patients. This therapeutic approach has great potential to restore neuronal activity in Parkinson's-affected circuits. There are currently several ongoing clinical trials with LRRK2 inhibitors, and we hope that these results in mice can be translated to humans,' says Pfeffer. The authors stress that, to maximize the effectiveness of this treatment, it is essential to identify early symptoms, which can occur up to 15 years before the characteristic tremors. The hope is that people with the LRRK2 mutation will be able to start treatment early. The next step would be to assess whether other Parkinson's variants, not associated with this genetic mutation, could also benefit from this strategy. It is estimated that the number of Parkinson's cases worldwide could exceed 25 million by 2050, which would represent a 112 percent increase over 2021 figures, according to projections published in the British Medical Journal. Although these estimates are not definitive, the scientific community warns that they reflect a growing challenge for public health systems. For this reason, developing therapies capable of mitigating, stabilizing, and even reversing the progression of the disease is a global priority. This story originally appeared on WIRED en Español and has been translated from Spanish.
