The #1 Habit to Break to Reduce Visceral Fat, According to Dietitians

 My social connections and travel have taken precedence over exercise right now. But having a four level condo means I'm doing lots of steps daily.

The #1 Habit to Break to Reduce Visceral Fat, According to Dietitians

Say goodbye to stubborn belly fat. No gimmicks, diets or gym memberships required!

Reviewed by Dietitian Mandy Enright, M.S., RDN, RYT

Spending too much time being sedentary is the number one habit to break to burn visceral fat.

• Smart exercise strategies such as starting small, setting a timer and variety can help.
• Nutrition, sleep and stress management are all helpful in reducing visceral fat.

The Plank Challenge may be all over social media. But there’s another reason to burn off belly fat that has nothing to do with sculpting killer abs. Belly fat, technically known as visceral fat, can spell bad news for your health. 

If you’ve never heard of visceral fat before, this type of fat burrows deep into your abdomen, where it surrounds organs like the liver and intestines. That doesn’t just make your belly rounder. Visceral fat also cranks out inflammatory proteins that increase the risk of chronic illnesses like heart disease, diabetes, nonalcoholic fatty liver disease and some cancers.

However, your lifestyle habits can have a big impact on the amount of visceral fat you carry. If you’d like to trim belly fat and improve your health in the process, read on to learn the No. 1 habit to break to reduce visceral fat.

Being Too Sedentary is the Biggest Habit to Break

If you’re sitting down reading this, then stand up immediately. Then get ready for this … being too sedentary is the No. 1 habit you need to break ASAP to reduce visceral fat. 

Why? Most of us are not nearly active enough (and spend way too much time sitting!). While physical activity guidelines recommend engaging in at least 150 minutes of activity per week, less than half of us actually meet these recommendations. 

Related video: 8 tips to lose belly fat faster (super easy!) (BarbarianBody) 

Yet, research reveals that increasing physical activity may be one of the best ways to stop the progression of diseases triggered by excess body fat. “By increasing movement, you can build lean body mass, which helps to increase overall resting metabolism, promoting more favorable body composition,” says Erin Palinski-Wade, RD, CDCES. “Movement also enhances fat metabolism and regulates insulin levels, helping the body burn stored fat more effectively.”

Exercise Strategies On How to Reduce It

Burning visceral fat may require some strategies. Here are some expert tips on how to do it:

• Start Small: Visceral fat may be stubborn, but you don’t have to run a marathon to get rid of it. “If you're new to regular movement, start with just 10 to 15 minutes of an activity you enjoy, like a walk around your neighborhood, dancing or yoga,” says Patricia Bannan, M.S., RDN. “Fit in movement throughout the day in small ways, such as taking the stairs instead of the elevator, parking farther away, or taking the long way to the coffee machine at work to add more steps to your day,” adds Palinski-Wade.
• Buddy Up: The best way to make it a habit is to repeat it daily until it’s as normal as brushing your teeth. Bannan recommends teaming up with a friend to make your movement habit stick. “Celebrating small wins, like reaching a daily step goal, can build momentum and make it easier to stay active in the long term,” she says.
• Set a Timer: “Every 30 to 60 minutes, set a reminder to stand up, stretch or walk around for a couple of minutes,” says Bannan. “This breaks up long periods of sitting and helps stimulate circulation and muscle activity.”
• Pace Around the House: Palinski-Wade recommends walking while talking on the phone instead of sitting. “This way you are using time you already have to fit more movement into your busy day,” she adds.
• Pump Some Iron: “Strength training is one of the best things you can do to offset visceral fat,” says Palinski-Wade. “Aim to add strength training one to two times per week, focusing on major muscle groups to improve strength and lean body mass.”
• Mix Up Your Workouts: Strength training isn’t the only way to burn visceral fat. Research has found that three aerobic or interval workouts per week are also effective for reducing belly fat.

Other Tips for Reducing Visceral Fat

Yes, moving is key, but there are even more steps you can take to lose visceral fat. 

• Log Those Zzz’s. “Just one poor night of sleep can increase appetite and insulin resistance, making you more likely to eat excess calories and triggering your body to store more visceral fat versus burning it,” says Palinski-Wade. In addition to practicing good sleep hygiene, these healthy sleep habits can also help with weight management.
• Chill Out. “Mindfulness activities, such as mindful eating or stress-reducing practices, like meditation or deep breathing, can help lower cortisol levels, a hormone linked to visceral fat accumulation,” says Bannan. “Managing stress through mindfulness can be an effective way to support your body’s ability to burn fat, particularly in the abdominal area.” 
• Enlist Fiber. “Adding more fiber to your diet can help to balance blood sugar, which in turn can lessen insulin resistance that stores visceral fat,” says Palinski-Wade. “In addition, dietary fiber helps to curb appetite and may promote weight loss, further lowering visceral fat levels.” Plus, high-fiber foods are often rich in antioxidants, which may offset inflammation and reduce stress hormones.
• Don’t Skimp on Fat. It may sound counterintuitive, but in order to lose visceral fat, you have to eat healthy fats. “Fatty fish is rich in omega-3 fatty acids, which have been shown to reduce inflammation and improve fat metabolism,” says Bannan. “Including salmon or other fatty fish, like mackerel, sardines, herring or trout in your diet a couple of times a week can support your efforts to reduce visceral fat while also promoting heart and brain health.”

Our Expert Take

There’s no magic pill to reduce visceral body fat. However, nutrition experts agree that simply moving more can improve your body composition and reduce visceral body fat. And you don’t have to log hours in the gym to see results. While strength training and aerobic activity are excellent ways to burn belly fat, going for regular walks with a friend or scheduling movement breaks into your workday are great ways to incorporate more activity into your day. The goal is to rack up those 150 minutes of physical activity each week. And if you still want to do the Plank Challenge, well, that’s great too!

Read the original article on EatingWell

These Midlife Heart Markers Predict Who Lives to 90 (and Enjoys Their 80s) by Super Age

 No smoking - Yes

BMI - I'm ignoring this, mine is 28.3

Blood pressure - usually 140 with meds when I donate blood, not concerned.

Cholesterol - No clue, don't care.

Blood sugar - 5.7, mildly elevated will get a finger monitor to track my levels

I will easily get to my 90s and beyond, genetics are very good, Dad died at 91 from Parkinsons and dementia, Mom at 97 still living alone at home, no longer driving and staying on the main level of the house. 

These Midlife Heart Markers Predict Who Lives to 90 (and Enjoys Their 80s)

These 5-Second Hand Exercises For Dementia Are Going Viral. Here's What A Neurologist Thinks.

 My incompetent everyone COMPLETELY FAILED at curing my spasticity and getting my left hand functioning again. Nothing here will help me. 

These 5-Second Hand Exercises For Dementia Are Going Viral. Here's What A Neurologist Thinks.

Social media is full of health hacks for better sleep, clear skin, a functioning gut, you name it. Lately, a tip for aging and cognitive function is gaining traction. 

Videos showing hand and finger exercises have racked up millions of views on TikTok and Instagram, with users suggesting these movements can help prevent dementia or Alzheimer’s disease.

The exercises include things like alternated clapping, tapping, arm circles and pointing your fingers in different directions. And although they might look easy enough, exasperated folks in the comments sections highlight that some of these motions are a lot harder than they appear. 

But does failing at intricate finger movements and hand coordination exercises mean you’re cognitively doomed? And can these exercises really ― as the captions claim ― prevent dementia or Alzheimer’s? HuffPost asked a neurologist to weigh in. 

“While there are a few studies showing that aspects of mild cognitive impairment might be improved with these types of hand exercises, I would put forward that there is nothing magical about these movements,” said neurologist Dr. Chris Winter.

Hand exercises are a way to practice motor skills, which can be beneficial for maintaining cognitive abilities as we age. But it might be a stretch to suggest that specific movements are going to remove your risk of developing dementia or Alzheimer’s disease. 

Winter explained that hand and finger coordination can be beneficial as part of a larger pattern of mental and physical activity, but it’s not the hand gestures themselves that matter ― it’s the engagement and concentration involved.

“Learning to play the piano or other activities that force concentration and the practice of improved hand/eye coordination are potentially just as useful,” Winter said. “I recommend that people stay active and engage in appropriately challenging activities. Learn a new language, pick up a guitar or a used set of drums, play pickleball. If you have the capacity to do these things, get off of TikTok and go do these things instead.”

Related video: Research reveals the habits scientifically proven to add a decade to your lifespan (Talking With Docs)

Brain function is less about hand gestures and more about movement and mental engagement that challenge your mind and body overall. 

Winter also emphasized that TikTok viewers shouldn’t mistake their inability to do some of these hand exercises as a red flag for cognitive decline. If you have trouble alternating pointing your thumbs and pinkies, that doesn’t mean you’re “already developing dementia,” as some commenters fear. 

“I think there are a variety of reasons why one could not do these gestures ― or rub their stomach while patting their head,” he said. “While someone with significant dementia is probably not likely to be able to do these activities, the fact that someone struggles with coordination does not indicate dementia or progression in this direction. Ability to pat your hands together is not a diagnostic test for cognitive decline.”

So while those quick coordination challenges might be fun or stimulating, experts say, your best bet for brain health still lies in the basics: regular exercise, quality sleep, a balanced diet and staying mentally and socially active. And what exercise and mental stimulation mean can vary based on individuals’ abilities. 

Health: The U.S. Is Experiencing 'National Trauma' — And It Explains Why So Many Of Us Feel Miserable

“If you only have the capacity to practice hand gestures, then that’s OK too,” Winter said. 

But just remember that the real “hack” for keeping your brain sharp isn’t a social media exercise ― it’s a holistic approach to living a healthy, mindful and engaged life. 

Related...

• 'Friluftsliv' Might Be The Scandinavian Habit You Need To Have A Better Fall And Winter
• Therapists Warn This Normalized Trump Behavior Is Causing Real-World Harm
• This Thumb Test May Indicate If You're At Risk For A Heart Problem
• Dementia Researchers Discover 2 New Dementia Risk Factors — Here's What They Are
• 8 Simple Exercises That Can Do Wonders For Your Sex Life

Read the original on HuffPost

Your brain changes at 9, 32, 66, and 83

 I think I went right past the age 66 one and will totally bypass the 83 one also.

Your brain changes at 9, 32, 66, and 83

Brain scans of 3,802 people show how the brain’s structure changes at four major turning points.

A team of neuroscientists at the University of Cambridge in the United Kingdom identified five broad phases of brain structure over the course of an average human life. These eras occur as the human brain rewires to support the different ways of thinking while we grow, mature, and eventually decline. The five major turning points are detailed in a study published today in the journal Nature Communications.

In the study, they compared the brains of 3,802 people between ages zero and 90, using datasets of MRI diffusion scans. These types of MRIs map neural connections by following how water molecules move through brain tissue. They detected five broad phases of brain structure in the average human life that are split up by four pivotal turning points between birth and death when our brains reconfigure. 

The major turning points occur at ages: 

• Nine (Childhood brain architecture)
• 32 (Adulthood brain architecture) 
• 66 (Early aging)
• 83 (Late aging)

“We know the brain’s wiring is crucial to our development, but we lack a big picture of how it changes across our lives and why,” study co-author and neuroscientist Dr. Alexa Mousley said in a statement. “This study is the first to identify major phases of brain wiring across a human lifespan. These eras provide important context for what our brains might be best at, or more vulnerable to, at different stages of our lives. It could help us understand why some brains develop differently at key points in life, whether it be learning difficulties in childhood, or dementia in our later years.” 

Related video: The 3 ages that change your body the most, according to science (En Pareja)

Age nine–From baby to kid

From infancy through early childhood, the brain is defined by network consolidation. All of the connectors between neurons called synapses that were overproduced in a baby’s brain whittle down. The more active synapses survive, shaping the brain’s early architecture. 

Across the whole brain, these connections rewire in the same pattern from birth until about nine years old. Meanwhile, the brain’s grey and white matter grow rapidly in volume.

The childhood brain runs from birth up until a turning point at the age of nine. Here, the brain is experiencing a change in cognitive capacity, but also an increased risk of mental health disorders. 

Age 32–Adult brain takes shape

In the early 30s, the brain’s neural wiring shifts into adult mode. White matter continues to grow in volume, so the brain’s communications networks are increasingly refined based on MRI scans showing how water molecules movies. These changes keep the brain at an enhanced level of cognitive performance that peak in the early 30s and is the brain’s “strongest topological turning point” of the entire lifespan, according to the team.

Around the age of 32, we see the most directional changes in wiring and largest overall shift in trajectory, compared to all the other turning points,” said Mousley. “While puberty offers a clear start, the end of adolescence is much harder to pin down scientifically. Based purely on neural architecture, we found that adolescent-like changes in brain structure end around the early thirties.”

Adulthood is the longest era and three decades. The brain’s architecture also stabilizes compared to previous phases, without any major turning points for the next 30 years. According to the team, this corresponds with a “plateau in intelligence and personality.”

Age 66–Early aging begins

This mid-60s turning point marks the start of an “early aging” phase of brain architecture. It’s a more mild period and is not defined by any major structural shifts. However, the team still  uncovered meaningful changes to the pattern of brain networks on average at around age 66.

The data suggest that a gradual reorganisation of brain networks culminates in the mid-sixties,” said Mousley. “This is probably related to aging, with further reduced connectivity as white matter starts to degenerate. This is an age when people face increased risk for a variety of health conditions that can affect the brain, such as hypertension.”  

Age 83–Late aging

The last turning point comes around age 83. The data for this final era is more limited, but the  defining feature is a shift from global to local. Whole brain connectivity declines even further and it relies on certain regions as others fade.  

“Looking back, many of us feel our lives have been characterised by different phases. It turns out that brains also go through these eras,” added study co-author and neuroscientist Duncan Astle. “Many neurodevelopmental, mental health, and neurological conditions are linked to the way the brain is wired. Indeed, differences in brain wiring predict difficulties with attention, language, memory, and a whole host of different behaviours”

Understanding that our brain’s structure journey is generally one of a few major turning points instead of a steady progression can help neuroscientists better identify when and how the wiring is more vulnerable. 

The surprising link between the size of your thighs and how long you'll live

 Which means your competent? doctor has to recover you 100% so you don't lose any muscle mass. Ask your doctor for specifics so you know what size thighs you need!

Can't or won't do that: PURE INCOMPETENCE!

The surprising link between the size of your thighs and how long you'll live

It turns out, thicker thighs may actually be the key to a long, healthy life.

Researchers have linked greater thigh strength and size to lower risks of heart disease, diabetes, cognitive decline and overall death. 

The thigh muscles, including the quadriceps, are among the body’s largest and most powerful muscles. They power everyday movement while helping support and protect our joints.

Beyond supporting everyday mobility, strong thighs may serve a greater purpose - better overall health and a longer lifespan. 

A five-year study published in The American Journal of Medicine examined the link between thigh strength and mortality in people with coronary artery disease (CAD), a condition in which plaque builds up in the arteries that supply blood to the heart.

Researchers studied 1,314 people with coronary artery disease, mostly men with an average age of 65, who had been hospitalized or undergone surgery for the condition.

Participants' quadriceps strength was measured using a dynamometer, a device that measures force, by having them push as hard as they could against it with their legs. 

They then compared leg strength with body weight to see how strong each participant’s legs were for their size. 

Researchers tracked the participants for the next five years, and during that time period, 118 people died from any cause, including 63 from cardiovascular disease.

The team discovered that people with 10 percent greater relative leg strength (leg strength compared with their body weight) had a 23 percent lower risk of death overall, and a 34 percent lower risk of dying from heart-related causes.  

Related video: Why your exercise could be doing more harm than you think (Talking With Docs)

 'Skeletal muscle weakness promotes exercise intolerance and physical inactivity. Reduced physical activity itself has been shown to be an independent risk factor for cardiovascular disease and frailty,' the study stated.

The research added: 'Importantly, resistance training can enhance muscle strength, muscle mass, and functional capacity.'

Thigh size may also protect against serious health problems. A 2020 study published in Endocrine Connections linked larger thigh circumference to lower odds of high blood pressure, particularly in overweight people. 

Researchers recruited 9,520 adults aged 40 and older from a larger Chinese community. They measured both thighs and took the average circumference. 

Participants' blood pressure was measured three times, with the average recorded. They were then split into three groups based on thigh size - small, medium and large - and had their blood pressure compared.

The rate of high blood pressure generally fell as thigh size increased, especially among overweight and obese people in the study.

The research, published in Journal of Lifestyle Medicine, evaluated 1,508 participants' leg strength using a dynamometer. 

They were then given a two minute cognitive test, where they matched specific symbols to numbers using a provided reference key.

The participants' scores were compared and researchers found that people with stronger legs performed better on the cognitive test.

To improve overall health and wellbeing, the best way to build thigh muscle is through strength training.

Compound moves like squats, leg presses, deadlifts and lunges can build muscle to support everyday movement, especially as you age. Aerobic exercises like cycling, walking and yoga can also improve flexibility, mobility and endurance. 

Read more

LVADs Linked to Concerning Neurologic Events, Strokes Aside

 If your doctors suggest this, have THEM GUARANTEE no complications! Can't do that, what is the backup plan?

An LVAD (left ventricular assist device) is a surgically implanted mechanical pump that helps a weakened heart pump blood to the rest of the body.

LVADs Linked to Concerning Neurologic Events, Strokes Aside

 Subarachnoid hemorrhage, subdural hemorrhage, encephalopathy emerge in registry data

Key Takeaways

• A registry study found an 8% incidence of stroke at 1.4 years after LVAD placement, accompanied by another 8% incidence of nonstroke neurologic adverse events.
• Pre-LVAD extracorporeal membrane oxygenation (ECMO) and concomitant surgery may be modifiable targets to reduce neurologic dysfunction.
• A more complete view of neurologic dysfunction is needed to inform decision-making, researchers said.

It's not all about stroke: Various neurologic events boded poorly for survival on the contemporary magnetically levitated HeartMate 3 left ventricular assist device (LVAD) in a retrospective registry study.

Based on the U.S. INTERMACS database, there was an 8% incidence of both stroke and nonstroke neurologic adverse events (NAEs) over a median 1.4 years among nearly 12,000 people with advanced heart failure who got the contemporary magnetically levitated LVAD.

Two-year survival rates were 45% in LVAD recipients who had a stroke and 56% in peers with nonstroke neurologic events (P<0.001). Compared with no neurologic event, there was an elevated risk of death after a stroke (HR 7.3, 95% CI 6.6-8.1) or a nonstroke neurologic event, the latter associated with:

• Highest mortality risk where there is overt central nervous system (CNS) injury (HR 12.58, 95% CI 10.39-15.23)
• High risk with covert CNS injury detected by neuroimaging (HR 9.19, 95% CI 6.75-12.51)
• Lower but still elevated risk with neurologic dysfunction without CNS injury, such as encephalopathy (HR 3.69, 95% CI 3.20-4.25)

"Stroke and nonstroke NAEs are incurred by a similar proportion of patients, and both are associated with substantially reduced survival. Consequently, stroke and nonstroke NAEs should be given comparable weight with universal nomenclature when evaluating the safety of durable LVADs," concluded a group led by Omar Saeed, MD, MSc, of Montefiore Medical Center, Albert Einstein College of Medicine in New York City, reporting in JACC: Heart Failure.

In their study, there were two potentially modifiable targets to reduce neurologic dysfunction from LVAD therapy: pre-LVAD extracorporeal membrane oxygenation (ECMO) and concomitant surgery.

A Long List of Neglected Neurologic Complications?

Much attention has centered strokes as the neurologic complication of concern in LVAD recipients. Prior work established that strokes may arise due to thromboembolism from various sources, while preexisting cerebrovascular disease, uncontrolled hypertension, and anticoagulation therapy may also contribute to stroke burden, Saeed and colleagues noted.

Other clinically significant neurologic complications, such as encephalopathy, have consequently been less well described.

"Neurological assessment after LVAD implantation should extend beyond focal stroke symptoms," commented Sung-Min Cho, DO, MHS, of Johns Hopkins University School of Medicine in Baltimore, who was not involved with the study.

Of note, Cho told MedPage Today, it may not be the case that encephalopathy itself causes death, as it may reflect underlying infection, shock, or multiorgan dysfunction. "Altered mental status/encephalopathy may warrant clinicians' attention both to possible brain injury and to the systemic illness that may be causing it, both of which increase the risk of death."

There is also an issue with attributing deaths to covert brain injury, as scans are ordered usually when a patient is already doing poorly, according to Mandeep Mehra, MD, MSc, of Brigham and Women's Hospital and Harvard Medical School in Boston, who was also not involved with the study.

Cho and Mehra both stressed the clinical heterogeneity of the so-called "nonstroke" endpoint in the study, which included overt CNS injury from subarachnoid hemorrhage (SAH), hypoxic-ischemic injury, subdural hemorrhage (SDH), or traumatic brain injury; covert CNS injury detected by neuroimaging; and neurologic dysfunction without CNS injury including encephalopathy, delirium, seizures, and transient ischemic attacks (TIA).

"SAH is a cerebrovascular event ordinarily considered a hemorrhagic stroke; SDH is generally classified separately, but grouping both under 'nonstroke neurological dysfunction' obscures the distinction between structural brain injury and conditions such as delirium in my opinion," Cho said.

"The nonstroke category needs dissecting before we give it equal weight with stroke. Seventy percent of these events are encephalopathy, delirium, seizures, or TIA. None of them were adjudicated, and in a very sick postoperative patient they are often a consequence of sepsis or multiorgan failure rather than a device-related brain injury," warned Mehra. "What we need is rigorous, adjudicated, device-attributable neurological endpoints. Lumping heterogeneous, unadjudicated events into a safety endpoint for future device trials could obscure rather than clarify device performance."

Can Neurologic Events Be Prevented?

Saeed's group performed a retrospective cohort study using the nationwide Society of Thoracic Surgeons INTERMACS database. Included were 11,739 patients who got a HeartMate 3 LVAD from 2017 to 2023.

The authors reported that pre-LVAD ECMO was associated with more stroke (HR 1.70, 95% CI 1.35-2.16) and nonstroke events (HR 1.45, 95% CI 1.11-1.90); concomitant surgery was also tied to stroke (HR 1.23, 95% CI 1.08-1.41) and nonstroke events alike (HR 1.17, 95% CI 1.03-1.34).

"Patients coming to implant on ECMO or temporary support, or undergoing concomitant procedures, carry higher neurological risk. That calls for careful thrombus screening, attention to stasis, and early neurological assessment after surgery," Mehra said.

Cho and Mehra both cautioned against calling ECMO a "modifiable" risk factor based on these findings, however. "Patients are on ECMO because they are in shock. ECMO marks severity of illness more than it represents a choice we can simply avoid," Mehra said.

It also remains to be shown that "avoiding ECMO would reduce neurological injury," according to Cho.

In any case, there is already some improvement on the neurologic safety of LVADs, as Saeed and colleagues reported that stroke and nonstroke NAEs occurred at an incidence of 0.044 and 0.049 events per patient-year, respectively, in this real-world cohort. In contrast, in the MOMENTUM3 trial, the incidence of any stroke was 0.050 events per patient-year across HeartMate 3 and HeartMate II LVAD recipients, while other neurologic events were logged at 0.073 events per patient-year.

The contemporary HeartMate 3 is already an improvement over its predecessor HeartMate II in terms of staving off neurologic complications. In a prespecified analysis of MOMENTUM 3, stroke rates were 10.1% and 19.2% in the first 2 years between the two LVAD groups, respectively (P=0.02).

"I was not at all surprised by this analysis which is itself reassuring(I'm not reassured at all, you are not the one under the knife!)," and "confirms that neurological complications have fallen substantially in the magnetically levitated era," said Mehra. "The device itself is no longer the dominant driver of neurological risk; the surgery and peri-implant factors are the issue."

The report found that the independent predictors of death after stroke were older age, pre-LVAD implantable cardioverter-defibrillator, higher pre-LVAD blood urea nitrogen level, and pre-LVAD dialysis. Predictors of death after nonstroke NAE were higher pre-LVAD body mass index, higher pre-LVAD serum creatinine, greater pre-LVAD international normalized ratio, and lower pre-LVAD albumin.

"Awareness of these patient-level characteristics may help direct resources to those who are most vulnerable after the occurrence of NAEs," the study authors suggested.

Saeed and colleagues nevertheless acknowledged that their retrospective study left room for bias and did not account for variables such as blood pressure management, anticoagulation management, or atrial fibrillation. Additionally, NAE events may be underestimated due to the lack of reporting of recurrent events and the classification of patients experiencing both stroke and nonstroke NAEs as stroke only.

Microglia Rescue Vulnerable Dopamine Neurons in Parkinson’s

 With your risk of Parkinsons' poststroke. How is your competent? doctor ensuring these microglia are working in your case?

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here: 

Microglia Rescue Vulnerable Dopamine Neurons in Parkinson’s

Summary:

Researchers at the University of Oxford have discovered that human microglia can selectively prune away toxic alpha-synuclein aggregates from dopamine-producing neurons without destroying the host nerve cells. Utilizing co-cultures of human induced pluripotent stem cell (iPSC)-derived neurons and microglia, the team demonstrated that microglia employ “trogocytosis”, a precise cellular nibbling mechanism, regulated by GPNMB, P2RY12, and CD22 signaling pathways, along with an IL-10 molecular brake. The findings identify a distinct, neuroprotective microglial subtype that shields neurons in Parkinson’s disease.

Key Facts:

• Selective Pruning via Trogocytosis: Human microglia selectively extract and dispose of aggregated alpha-synuclein clumps by “nibbling” specific segments of living dopamine neurons while preserving overall neuronal viability and connectivity.
• GPNMB Identified as Functional Driver: Glycoprotein non-metastatic melanoma protein B (GPNMB), a protein previously linked to Parkinson’s risk via genome-wide association studies (GWAS), binds directly to alpha-synuclein and is required for microglia to effectively clear aggregates.
• Fine-Tuned Immune Brakes: The protective clearance mechanism is controlled by sensing receptors (P2RY12), inhibitory checkpoints (CD22), and an interleukin-10 (IL-10) autocrine brake that prevents runaway neurotoxic inflammation.

Source: University of Oxford

Beyond the Double-Edged Sword: A Precision Immune Defense

In neurodegenerative diseases, microglia, the central nervous system’s resident immune sentinels, are typically framed through a conflicted narrative. Under physiological conditions, they survey brain tissue, prune synapses, and clear cellular debris; during chronic neurodegeneration, their persistent activation drives inflammatory signaling cascades that accelerate neuronal death.

Nowhere has this paradox been more evident than in Parkinson’s disease, a condition affecting more than 10 million individuals globally. The disease is defined by the selective death of dopamine-producing neurons within the substantia nigra, driven largely by the misfolding and aggregation of alpha-synuclein into toxic intracellular clumps.

Whether human microglia can intervene constructively to rescue dopamine neurons from this proteinaceous burden, without destroying the neurons in the process, has remained an open question.

Now, a team of neuroscientists at the University of Oxford has revealed an unexpected, highly targeted defense mechanism.

The researchers established that a specialized population of human microglia actively extracts and destroys harmful alpha-synuclein aggregates directly from living dopamine neurons via trogocytosis (from the Greek trogo, meaning “to gnaw” or “to nibble”).

“What is striking is the precision of this response,” said first author Hung-Ju Chueh, Ph.D., of the University of Oxford. “The microglia were not simply engulfing damaged neurons but instead removing parts of the neuron containing aggregated alpha-synuclein, suggesting that, at certain stages of disease, microglia help neurons dispose of potentially harmful material.”

Engineering Human iPSC Co-Cultures to Model Live Interactions

To investigate interactions between human brain cells in real time, the Oxford investigators generated human induced pluripotent stem cell (iPSC) lines, co-culturing authentic human dopamine neurons alongside human microglia.

The team modeled alpha-synuclein pathology through two complementary methods: by introducing genetic alpha-synuclein gene dosage elevations (triplication), and by seeding the cultures with exogenous preformed alpha-synuclein fibrils that template the misfolding of native neuronal protein.

High-resolution cellular imaging revealed that rather than engulfing entire dying neurons via standard phagocytosis, the microglia selectively nibbled off membrane pockets enclosing the aggregated protein. This process of trogocytosis eliminated the toxic pathology while leaving the broader axonal network and cell body intact.

Single-cell RNA sequencing showed that this clearance was driven by a distinct, transcriptionally defined subpopulation of activated microglia. This subset was kept from over-activating through a balanced signaling network:

• Surveillance and Guidance: Governed by P2RY12 purinergic receptor sensing.
• Cellular Checkpoints: Regulated by CD22 inhibitory surface interactions between neurons and microglia.
• Inflammatory Suppression: Maintained by an autocrine interleukin-10 (IL-10) brake that halted secondary, collateral inflammatory tissue injury.

Solving the GPNMB Genetic Mystery in Parkinson’s

The investigation also cracked a longstanding genetic puzzle. Multiple large-scale genome-wide association studies (GWAS) had previously flagged variants in the GPNMB (glycoprotein non-metastatic melanoma protein B) gene locus as significant risk factors for Parkinson’s disease, but its mechanistic function in the brain remained unknown.

The Oxford team discovered that GPNMB is directly upregulated in human microglia when exposed to aggregate-bearing neurons, where it physically interacts with pathological alpha-synuclein within the microglial machinery.

Furthermore, post-mortem analysis of human brain tissue from patients with incidental Lewy body disease and confirmed Parkinson’s disease revealed elevated GPNMB levels within substantia nigra microglia.

To confirm causality, the team used CRISPR interference (CRISPRi) to knock down GPNMB expression in human microglia. Deprived of GPNMB, the microglia lost their ability to clear alpha-synuclein aggregates from the neighboring dopamine neurons, establishing GPNMB as an essential driver of the neuroprotective response.

“Our findings highlight that the immune response in Parkinson’s disease is more nuanced than simply being beneficial or harmful,” noted senior author George Tofaris, M.D., Ph.D., Professor of Neurology and Translational Neuroscience at the University of Oxford. “We have identified a population of human microglia that can actively remove pathological alpha-synuclein from neurons. Understanding how to enhance and monitor such beneficial microglial functions, without triggering damaging inflammation, could open up new avenues for developing disease-modifying treatments.”

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this Neurology Research:

• Media Contact: Christopher McIntyre
• Source: University of Oxford
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Science Translational Medicine (Oct 7, 2026). “Human microglia clear intraneuronal alpha- synuclein aggregates by GPNMB-mediated trogocytosis.” Authors: Hung-Ju Chueh, Antigoni Katsikoudi, Ana Aragón-González, Chor Lai Lam, Liezel Tamon, Ashwin Jainarayanan, Devika Agarwal, Sally A. Cowley, David Sims, and George K. Tofaris.
• DOI: 10.1126/scitranslmed.adz9258

Statins Linked to Reduced Glaucoma Risk and Slower Progression

 

 Your competent? doctor immediately prescribed statins post stroke based on earlier research, right? NO? And still hasn't been fired yet?

1. Statins.

tested in rats from 2003

http://Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke  

Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice

Or,

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons 

October 2012

tested in humans, March 2011

http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html

And now lost even to the Wayback Machine

So, I think this below is the actual research.

Association Between Acute Statin Therapy, Survival, and Improved Functional Outcome After Ischemic Stroke April 2011 

The latest here: 

Statins Linked to Reduced Glaucoma Risk and Slower Progression

Summary:

A massive real-world epidemiological investigation from the UC San Diego School of Medicine reveals that statin medications are associated with a significantly reduced risk of developing open-angle glaucoma and a lower rate of surgical escalation in those already diagnosed.

Analyzing health records from more than 420,000 propensity-matched individuals across a 20-year cohort in the British Journal of Ophthalmology, researchers discovered that statin users had a 15% lower incidence of glaucoma and up to a 55% to 60% reduction in the need for laser or surgical interventions.

Key Facts:

• Lower Glaucoma Incidence: Statin use was associated with a 15% relative risk reduction in developing open-angle glaucoma compared to matched non-users over five years.
• Significant Reduction in Surgical Escalation: Among patients with established glaucoma, statin therapy was linked to a 36% lower risk of incisional surgery, a 55% reduction in minimally invasive glaucoma surgery (MIGS), and a 60% reduction in selective laser trabeculoplasty (SLT).
• Massive International Cohort: The study evaluated electronic health records from a global registry spanning 165 million patients, examining over 210,000 matched pairs followed between August 2006 and August 2026.

Source: UC San Diego School of Medicine / British Journal of Ophthalmology

Glaucoma is one of the leading global causes of irreversible blindness, marked by the progressive and permanent degeneration of retinal ganglion cells and optic nerve axons. While current clinical management focuses almost exclusively on lowering intraocular pressure (IOP) via topical eye drops, laser procedures, or invasive filtering surgeries, mechanical pressure reduction does not always halt neurodegenerative progression.

Statins, the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors taken by tens of millions of adults to manage cardiovascular disease, are increasingly recognized for their pleiotropic properties. Beyond reducing low-density lipoprotein (LDL) cholesterol, statins exhibit potent anti-inflammatory, antioxidant, endothelial-stabilizing, and neuroprotective activities across the central nervous system.

Whether these systemic actions translate into measurable clinical protection for the human optic nerve has remained an unresolved question in ophthalmic medicine.

Now, an observational study led by researchers at the University of California San Diego School of Medicine provides robust population-scale evidence that statins protect against both the development and the clinical progression of glaucoma.

Published online in the British Journal of Ophthalmology, the study shows that statin users not only develop open-angle glaucoma less frequently, but those already living with the condition are significantly less likely to require advanced interventions, such as laser therapy or operating room surgery.

“Glaucoma is one of the leading causes of irreversible blindness, and statins are among the most common medications used to lower cholesterol and reduce the risk of heart disease,” said senior study author Robert Weinreb, M.D., Distinguished Professor in the Viterbi Family Department of Ophthalmology at UC San Diego School of Medicine and Director of both the Hamilton Glaucoma Center and the Gleiberman Center for Glaucoma Research at the Shiley Eye Institute. “If this association is confirmed in future studies, it could have implications for a very large number of people.”

Mining 20 Years of Global Patient Data

To resolve conflicting conclusions from smaller prior trials, the UC San Diego team, collaborating with researchers from the University of South Florida and the University of Southern California, queried a federated global database covering 165 million individuals.

The investigators structured two targeted clinical cohorts:

• Primary Incidence Cohort: The team compared 210,000 adults with a confirmed record of statin use between August 2006 and August 2026 against a meticulously matched control group of 210,000 individuals with no history of statin exposure. Both groups had documented longitudinal ophthalmological examinations. Over five years, 2.3% of the statin cohort developed open-angle glaucoma compared to 2.6% of the control group, representing a statistically significant 15% reduction in incident disease.
• Disease Progression Cohort: In a secondary analysis, researchers tracked more than 30,000 individuals with pre-existing glaucoma taking statins compared with nearly 250,000 glaucoma patients not taking statins.

Shielding the Optic Nerve from Escalating Interventions

In patients already managing glaucoma, statin use was tied to a marked decrease in the need for escalating treatments across both five- and ten-year follow-up windows.

At the five-year mark, statin therapy was associated with:

• A 60% lower risk of undergoing selective laser trabeculoplasty (SLT), a laser procedure that enhances aqueous outflow.
• A 55% reduced risk of requiring minimally invasive glaucoma surgery (MIGS), keyhole microsurgical implants designed to reduce intraocular pressure.
• A 36% lower risk of undergoing traditional, incisional glaucoma surgeries (such as trabeculectomy or tube-shunt drainage implants).
• A 12% reduced risk of needing additional prescription intraocular pressure-lowering eye drops.

These protective associations persisted out to a decade of follow-up, suggesting sustained therapeutic benefit over time.

“Statins are known to have pleiotropic effects beyond cholesterol lowering, including anti-inflammatory and potential neuroprotective properties,” Dr. Weinreb explained. “This study suggests those effects could be relevant to optic nerve health, and future studies will be able to tell us if this is a causal, clinically actionable relationship.”

Caveats and the Path to Randomized Clinical Trials

Because this investigation was retrospective and observational, the authors emphasize that it cannot demonstrate direct causality. Residual confounding factors, such as socioeconomic status, exercise, diet, or overall medication adherence, could influence the observed outcomes.

Furthermore, the database lacked granular physiological metrics, such as baseline intraocular pressure measurements, visual field mean deviation scores, or specific surgical rationales, precluding researchers from verifying whether surgeries were omitted due to milder disease or patient choice.

Nevertheless, given the high safety profile, affordability, and widespread accessibility of statins, the findings provide a strong clinical rationale for prospective, randomized controlled clinical trials to test whether targeted statin regimens can serve as adjuvant neuroprotective therapies to preserve eyesight in glaucoma patients.

Funding: The research was funded, in part, by Research to Prevent Blindness.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this Visual Neuroscience and Neuropharmacology Research:

• Media Contact: Miles Martin
• Source: UCSD
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: British Journal of Ophthalmology (Oct 1, 2026). “Statin use is associated with lower risk of open-angle glaucoma incidence and treatment escalation.” Authors: Forest Lin, Alexander T. Hong, and Robert N. Weinreb.
• DOI: 10.1136/bjo-2026-330339