Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label don't listen to me. Show all posts
Showing posts with label don't listen to me. Show all posts

Sunday, June 7, 2026

What Brain Imaging Reveals About The Effects Of Light Alcohol Use by mindbodygreen

 If you insist on drinking, as I do, to prevent dementia via social connections then you will need your doctor to give you protocols on increasing cerebral blood flow. You can't use mine, I'm not medically trained. 

cerebral blood flow (51 posts to December 2015)

What Brain Imaging Reveals About The Effects Of Light Alcohol Use

Tuesday, May 26, 2026

“Use It or Lose It:” What This Popular Neurorehab Phrase Means by Flint Rehab

 

I absolutely hate these pontifications on nonuse. Solve the damn problem of dead brain rehab and this nonuse problem goes away. SOLVE THE CORRECT PROBLEM!

Damn it all, it is NOT learned nonuse. It is the actual inability to use it because of dead neurons. If you had dead brain rehab protocols, this fake learned nonuse idea would cease to exist!

A couple points I'd like to make on this:

1. I disagree on 'Use it or lose it' existing for stroke survivors. You can read all about my reasons for that in these 11 posts.

2. Exercising the dominant side increases recovery of the affected side. Post here:

Compensatory rehabilitation limits motor recovery after stroke

3. I consider this as a crutch for your stroke medical 'professionals' to blame you for not recovering just because THEY ARE COMPLETE FUCKING FAILURES AT PROVIDING 100% RECOVERY PROTOCOLS!

But I'm not medically trained so my points should not be listened to.  

The latest here:

“Use It or Lose It:” What This Popular Neurorehab Phrase Means

To help you understand this popular neurorehabilitation phrase, this article will discuss:

What “Use It or Lose It” Means           

To minimize losses after neurological injury, individuals must focus on promoting neuroplasticity to reorganize the central nervous system’s neural circuitry and restore compromised functions. One of the most effective ways to do this is to think “use it or lose it.” It simply means that in order to retain proficiency over a function, you must practice it regularly.

Every function you perform activates a unique set of neural pathways in the central nervous system (the brain and spinal cord). The most frequently activated neural pathways are strengthened and maintained, while those less frequently activated become neglected and forgotten.

This occurs because the central nervous system no longer senses a demand for those functions. Therefore, to be as efficient as possible and save energy for more in-demand functions, it will start to forget how to perform unused functions.

Consequently, prolonged disuse can lead to learned non-use, which refers to the conditioned suppression of affected body parts. For example, when the left arm is weakened by a stroke, individuals tend to compensate by using their unaffected right arm. Consistently using the unaffected arm leads to disuse of the affected arm until eventually, individuals forget how to use their affected arm.

The only way to prevent functions from worsening and becoming useless after a neurological injury is to use them. Repetitively practicing functions affected by neurological injury reinforces demand for them and encourages the central nervous system to reorganize those functions to unaffected regions of the brain/spinal cord. The more you practice affected functions, the stronger the newly rewired functions become.

Now that you understand what “use it or lose it” means, let’s discuss some other principles of neuroplasticity.

Other Principles of Neuroplasticity

While “use it or lose it” is one of the most popular principles of neuroplasticity, the other principles are equally as important to help you understand how to optimize recovery after neurological injury.

Other principles of neuroplasticity include:

  • Use it and improve it. In order to get better at a specific function, you must consistently practice it.
  • Specificity. The way you train impacts the nature of plasticity. For example, training specific hand movements will help improve hand function after stroke.
  • Repetition matters. To strengthen neural circuits for a function, you must repetitively practice that function.
  • Intensity matters. The intensity of your training impacts how quickly adaptive changes occur.
  • Time matters. Depending on how long it has been since your injury, you may experience different states of plasticity. For example, immediately after injury, the brain experiences a heightened state of plasticity. Therefore, individuals tend to see the most results in the first several months after their injury.
  • Salience matters. Your motivation to train impacts neuroplasticity. The more important training is to you, the easier it is for you to participate in it.
  • Age matters. Neuroplasticity occurs more readily in younger brains. However, the brain never runs out of neuroplasticity and there is hope for recovery at any age.
  • Transference. Promoting neuroplasticity within one set of neural pathways can promote neuroplasticity for similar behaviors. For example, practicing leg exercises can help improve your walking skills.
  • Interference. Learning compensation techniques can make it difficult to regain an affected skill.

As you can see, various factors impact how quickly neuroplasticity is activated in the central nervous system. Fortunately, the brain adapts throughout your entire life and even years after your injury, there is always hope for recovery.

Is It Possible to Regain Lost Functions?

man participating in physical therapy after neurological injury to promote "use it or lose it" recovery principle

While prolonged disuse of affected functions can lead to losing them, it is always possible to relearn them. Any function can be relearned; however, it will take time to re-establish neural pathways for it. In other words, you’ll likely have to start from the beginning to regain lost functions.

This can be achieved by focusing on consistent and repetitive practice. The more you practice, the more rewiring will occur and the stronger neural pathways for that function will become.

While the point of “use it or lose it” is to encourage you to use affected functions to avoid losing them, it is never too late to promote neuroplasticity and relearn them. Even if it has been years since you’ve used your affected body part, there is always hope for recovery.

Use It or Lose It: Key Points

Your brain is always adapting based on the behaviors you consistently perform. After a neurological injury, you may experience various impairments such as difficulties controlling your movements or poor memory.

In order to prevent these functions from worsening, think “use it or lose it.” The more you practice functions affected by neurological injury, the better the central nervous system will get at recognizing the demand for them and utilize neuroplasticity to make adaptive changes.

Even if you’ve “lost” a function due to years of disuse, there is always potential to relearn it by engaging in consistent and repetitive practice. We hope this article helped you understand what “use it or lose it” means and how to enforce it to optimize your recovery outcomes.

Flint Rehab is leading the way in neuro-rehabilitation with products that are backed by research and clinically proven to help you recover more effectively from stroke, TBI, and SCI.

Trusted by over 300+ rehab facilities and 10,000+ home customers.

Sunday, May 17, 2026

Are You Overlooking The Best Supplement For Brain Health? (creatine) by mindbodygreen

 You'll have to ask your competent? doctor for the specific research that points to brain benefits and have him/her deliver AN EXACT PROTOCOL  for your use. Not being able to do that IS PURE INCOMPETENCE!

Don't listen to me, I'm not medically trained.

Are You Overlooking The Best Supplement For Brain Health?

Wednesday, February 18, 2026

Is Eight Drinks a Week Too Much for Brain Health? Study Finds Out

 Only an association, so I'm not worrying since my dementia prevention is being vastly improved by social connections at bars.

(I completely disagree on this one. My social connections are great on jazz and trivia nights at local bars, and that is going to prevent dementia! But I'm not medically trained, so don't listen to me. I just read lots of research abstracts.)

Jazz on Sunday and Tuesday nights, Trivia on Thursday, All are at bars so alcohol is involved. I'm totally ignoring this shit from doctors and researchers!  Life is fun and I'm enjoying it

Is Eight Drinks a Week Too Much for Brain Health? Study Finds Out

Saturday, January 31, 2026

We may have been misled about red wine's connection to longevity

 My go to healthy drink is an espresso martini with added chocolate liqueur and maple syrup instead of simple syrup. 

Highlighted items below are in direct contradiction of these two pieces of research:

So WHOM TO BELIEVE?  I'm going for the most fun.

 Do you any explanation per this research? Do smarter people have less chance of dementia? I'm pretty sure I qualify.

Smarter People Tend To Drink More Alcohol. 

All the research proven benefits follow on my espresso drink. Don't listen to me, I'm not medically trained but love to tweak your medical 'professionals' into defending their ideas.

This line is great: The findings indicate that even the Espresso Martini cocktail contains the espresso's beneficial compounds - and can contribute to staving off dementia.

The latest here:

We may have been misled about red wine's connection to longevity

Dry January is a time when the “evils” of alcohol hover over us. The warnings about alcohol feel endless: it might increase your risk of dementia, it might cause cancer, it might kill you.

But if that’s all true, why do so many “Blue Zone” centenarians drink red wine? Why does the American Heart Association say a small amount might reduce your risk of heart attacks? And if it’s that bad, why does the research seem conflicted?

Must Read: The Trump Administration Wants You To Drink Whole Milk — Here's What Actual Health Experts Want You To Know Of course you should be drinking whole milk; reasons here: 

We asked experts to break down what we know about red wine — and alcohol in general — and its impact on lifespan. 

Why We Connect Red Wine With Longevity

In the popular Netflix documentary “Live To 100,” longevity researcher Dan Buettner showed the habits and environment of centenarians who live in the “Blue Zones.” These are places where people tend to live longer than the rest of the world. In two of those communities, Sardinia, Italy, and Ikaria, Greece, drinking red wine is an important daily ritual.

“The majority of people in the Mediterranean Blue Zones — who live up to 10 years longer than Americans do — are drinking a glass or two of local red wine daily, usually with a meal, family and friends. We don’t know if they are living longer because of the wine, the fellowship or the combination of both,” Buettner said in an email to HuffPost.

There may not be enough polyphenols in a glass of wine to make a difference, and cardiovascular impact has also been observed when people drink other types of alcohol.

 While this population tends to drink wine as they eat and socialize, they follow other healthy habits, too. Their diet is high in fruits and vegetables, they are close with family and friends, and they get regular exercise. It’s possible that these other practices outweigh the moderate indulgences. “It remains unknown whether drinking can be part of a healthy lifestyle,” saidDr. Mariann Piano, professor emeritus of nursing at Vanderbilt University. “Clearly, drinking too much — and that includes more than two drinks a day — is associated with many adverse cardiovascular effects. … I think the controversy is more around the low to moderate levels.”

Must Read: The Audacity Of Going To A Mexican Restaurant When You're An ICE Officer

Here’s The Controversy

Research clearly shows that excessive alcohol consumption and binge drinking can lead to medical issues, but the impact of lower quantities is more complicated.

Studies have shown that light drinkers may have lower mortality than both abstainers and heavy drinkers. Some researchers contest the finding, but Dr. Eric Rimm, a professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, attributes it to a reduced risk of cardiovascular disease.“It does look like people who drink half a drink to one drink a day, which means three to seven drinks a week, live the longest,” Rimm said. “Most of that is explained by the fact that they have lower rates of heart attacks — and heart attacks cause death.”

In fact, heart disease is the No. 1 cause of death in the developed world. 

Must Read: Your Choice Of Afternoon Snack Could Increase Your Risk Of Dementia

In June, the American Heart Association released a review showing that low levels of alcohol showed no risk, or potentially lowered risk, of cardiovascular conditions. In small amounts, it can raise good cholesterol, have a blood-thinning effect and lower blood pressure. This was not specific to red wine, though.

You may have heard that the polyphenols, or antioxidants, in red wine are what cause this, but this is unproven. There may not be enough polyphenols in a glass of wine to make a difference, and the cardiovascular impact has also been observed when people drink other types of alcohol.Your heart isn’t the only area of focus when it comes to your body’s reaction to alcohol. Small quantities may also reduce the risk of developing Type 2 diabetes. 

“Moderate alcohol, 5 to 10 ounces a day, has been shown to potentially reduce the risk of developing Type 2 diabetes. Interestingly, some of the studies showed patients even losing a few pounds over time. … And even in our diabetic patients, we’re seeing improvements in blood sugars with moderate alcohol use, in particular with red wine,” said Dr. Steven Zygmont, diabetes and metabolism endocrinologist with Crouse Health. 

Must Read: Shoppers Swear Employees At This Grocery Store Are Trained To Flirt With You

It’s possible that the polyphenols cause red wine to have a slightly better effect than other drinks, or it may be a result of the way that people typically consume red wine. 

Health practitioners have major concerns about communicating these findings, which can easily be misunderstood. 

“It’s a really tricky public health message because of all of the dangers of alcohol,” Rimm said. “It’s unlike other things in public health, because if you tell people, ‘you should have more fruits and vegetables,’ they’re not likely to binge on fruits and vegetables on Friday and Saturday. But alcohol has the problem that the pattern is probably equally as important as the amount,” Rimm said.


Given the addictive nature of alcohol, one glass of wine can easily become two or more. It’s a fine line: Drinking a little has a low risk, but increasing the amount can dramatically raise your risk.

Plus, regardless of the other health implications, alcohol — including wine — is a known carcinogen. So, while heart disease remains the leading cause of death, cancer follows closely in second place. When it comes to cancer risk, there’s no safe amount of alcohol. 

Must Read: You May Want To Think Twice Before You Eat Bagged Lettuce

“Risks related to cancer should not be ignored, and considered on an individual basis,” Piano said. “Some advice we give to people is, ’If you have a really strong family history of cancer, then you may want to have less or no alcohol. Everybody can choose to drink nothing; however, there are many lifestyle behaviors we can engage in to reduce our risk of chronic disease.”

How To Make Informed Choices

So, what does wine actually look like in the longevity picture? 

Keeping the science in mind while looking at the Blue Zones of Sardinia and Ikaria, we see a tradition of drinking wine with meals as part of an overall healthy lifestyle. Wine tends to be shared in social settings over food, which can limit amounts and slow the pace, easing the load as the body works to metabolize toxins. 

“I think [red wine] is more linked to other positive eating and physical activity behaviors,” Piano said, pointing to a study that found a small protective association with preferences for wine and consuming alcohol with meals. This could be due to slower alcohol absorption, and it might reflect the lifestyle choices of people who prefer red wine as their drink of choice. 

“There are just too many unknowns at this time, except that drinking too much (and that includes more than two drinks a day) is associated with a lot of adverse cardiovascular effects,” Piano said.

Even if there is a protective effect associated with wine, it has serious limits. While light drinkers may have reduced cardiovascular risk, heavier drinkers have a significantly increased risk of heart attack, high blood pressure or stroke. Light drinkers tend to have lower rates of cognitive decline, but heavier drinkers are more likely to develop dementia. Light drinkers are less likely to develop diabetes, but excess drinking is a significant risk factor for Type 2 diabetes.

In 2023, the Canadian Centre on Substance Use and Addiction tried to organize this risk into charts to help people understand the continuum, which you can see here.

“Alcohol use cannot be addressed with a blanket statement, which I know is what the public wants,” Piano said. “Nonetheless, from a public health perspective, it is important to highlight the risk of cancer and chronic diseases, with higher consumption linked to greater harm. Be more intentional and mindful about what you’re drinking. … People need to understand what their risk is, and then it’s going to be up to them.”

So, if you are going to drink, is red wine the best choice? It’s possible that wine may have a slight edge over other types of alcohol due to its composition, but its main advantage probably lies in the traditions that surround it. Although there’s no definitive answer, one thing is clear: If you’re going to indulge in red wine, keep portions small, because healthy food and good company seem to be far more important for longevity than wine alone. 


Sunday, January 4, 2026

Doctor's orders: Eat ice cream, and other tips for a long and healthy life

 I bet your incompetent? doctor will ignore this advice just like they ignored the dairy fat one!

dairy fat (40 posts to April 2016)

Doctor's orders: Eat ice cream, and other tips for a long and healthy life

It may not sound like a New Year's resolution, but Dr. Ezekiel Emanuel is serving up some unusual advice as you start out 2026: Eat your ice cream. "Ice cream will make you happy, and that's very important," he explained.

I asked, "Why would I live longer eating ice cream?"

"Ice cream is a good dairy product; it's got protein, its saturated fats are in a globule, so it doesn't affect you as much as saturated fats in meats and other things," he said. "Plus, you typically do it socially with someone else. And you know, being happy is a very important part of living a long time."

"I feel like your saying 'eat your ice cream' is like 'Don't stress out as much about life. Be more social,'" I said.

"We're here for only 75, 85, 90 years. You've got to make life enjoyable. You've got to make it fulfilling," he said.

Norah O'Donnell and Dr. Ezekiel Emanuel, author of

The prominent oncologist and health policy expert is taking a different approach in his new wellness book, called, "Eat Your Ice Cream: Six Simple Rules For a Long and Healthy Life" (to be published Tuesday by W.W. Norton & Co.). He said, "I want people to stop obsessing. make it part of your life. You should like exercising, you should like eating well. Otherwise, you're not going to do it for years and years and decades, which is what's necessary for a long, healthy life."

 / Credit: W.W. Norton & Co.

The doctor's health handbook does include the basics of what to eat, how to exercise, and the all-important reminder that sleep is fundamental to wellness. But it goes beyond that, with behaviors that include "Don't be a schmuck."

"One of the things that is I think core to the book is, stop doing things that aren't good for your health," Emanuel said. "'Don't be a schmuck' is my father's reference to us when we were being stupid. And so, there are lots of things that we do as human beings that can be schmucky: smoking, vaping, doing drugs, not taking your vaccines. I don't agree with the current administration, and they're dead wrong on this."

Also on the so-called schmuck list: alcohol.(I completely disagree on this one. My social connections are vastly improved on jazz and trivia nights at local bars, and that is going to prevent dementia! But I'm not medically trained, so don't listen to me. I just read lots of research abstracts.)

I asked, "This is what everybody wants to know about: the right amount of alcohol, or no alcohol?"

Emanuel said, "There has been a lot of research on alcohol, so here's the way I distill it: The safest level is probably zero. There are some studies, and we should be clear, where it's half a cup a day, three cups a week."

"Nobody drinks a half a glass of wine," I said.

"So, you drink every other day," Emanuel said. "On the other hand, 60, 65% of the public drinks. You're not going from 65% to zero. So, you have to give people reasonable advice. And the reasonable advice is, first of all, no binge drinking, that's really bad for you. Don't drink alone. That's really bad for you. If you're using alcohol as a lubricant for social interaction, which many people do, that's probably good; you're getting some benefit from the social interaction."(THIS!)

Social interactions – a consistent theme for Emanuel – is something he learned at a young age, growing up with brother Ari, a super-agent in Hollywood, and his other brother Rahm, the former mayor of Chicago and ambassador, who may be running for president of the United States.

I asked, "What is it that your parents taught all of you that has led you, I mean, you're all incredibly successful?"

"Now you're gonna make me cry," Emanuel said, "because every time I talk about my parents and our growing up, I tend to cry. They taught us how to be social and interact with people. They also taught us how to be responsible. One of the things my mom did in raising us is, you know, get out of the house and go occupy yourself. Rahm and I went to school, I was six in first grade, and he was in nursery school. I had to take him from school, walk two blocks across a busy street, get on a bus, pay the car fare, get off at the right spot. I learned a huge amount of responsibility, taking care of my brothers.

"The other thing I think they did, which was super-important for us, is we all slept in the same bedroom. We were a unit. Yes, we fought endlessly. And you know, I like to joke with people, we didn't go to bed until there was blood, you know, because of all the fights. But we were also each other's best friends."

His takeaway: relationships matter.

Emanuel also lists lifestyle choices he considers "anti-wellness," like chronic stress(Especially the stress of your incompetent? doctor not knowing how to get you 100% recovered!), a fast-food diet, social media, and dining alone.

"I think people would agree with all of those, with the exception of dining alone," I said. "A lot of people go to a restaurant or get home from work, and dine alone."

Emanuel said that should be an occasional thing: "Don't make it every day. And you know, if you find yourself dining alone, what you should do is call up a friend. If you're sitting at a bar, right, and you're dining there, ask the person next to you, you know, 'Have you been to this restaurant before? What do you do? Why are you here?' Yeah, strike up a conversation. We underplay those casual conversations and how important they are for us."

His book also discusses retirement: "Retirement leads to more rapid cognitive decline for people. I say to people, don't retire. And if you're gonna retire, you have to plan retirement well, so that you stay engaged, you stay mentally sharp. And that doesn't mean, 'Well, you know, I'm gonna try to play the saxophone one day.'"

"But Dr. Emanuel, a lot of retired people like to buy books, and watch 'Sunday Morning,'" I said.

"Well, if they're buying books and staying mentally engaged that way, if they're going to volunteer, say, or they're talking to friends, or they're taking up a new hobby seriously, all of that is excellent, highly endorsed," he replied.

"Meaning don't retire the mind, or retire your social engagement?"

"Yes, and it's very important, you've got to be deliberate about it. You can't let nature take its course."

So, what is his biggest piece of advice for us in 2026? "Build your social relationships," he said. "It's definitely the most important thing for long-lasting health and happiness."

READ AN EXCERPT: "Eat Your Ice Cream" by Ezekiel J. Emanuel, M.D.

WEB EXCLUSIVE: Extended interview - Dr. Ezekiel Emanuel (Video)

   
For more info:

Ezekiel Emanuel, M.D."Eat Your Ice Cream: Six Simple Rules for a Long and Healthy Life" by Ezekiel J. Emanuel, M.D. (W.W. Norton & Co.), in Hardcover, eBook and Audio formats, available via AmazonBarnes & 

Thursday, December 18, 2025

Scientists Just Discovered Why Some Brains Stay Decades Younger by Super Age

 My social connections are vast. Jazz on Sunday and Tuesday nights, Trivia on Thursday, All are at bars so alcohol is involved. I'm totally ignoring this shit from doctors and researchers! 

Safest level of alcohol consumption is none, worldwide study shows

This is what your doctor will use, no thinking required.

Oh well, I disagree. I'm using bar nights of jazz and trivia to vastly expand my social connections which is what is going to prevent dementia. You can't listen to me; I'm not medically trained. Better stroke recovery from music and better cognition from trivia; so there. 

The latest here:

Scientists Just Discovered Why Some Brains Stay Decades Younger

Sunday, November 23, 2025

Alzheimer’s Drug Reduces Amyloid but Fails to Restore Brain Waste Flow

 

Whoops, lecanemab is not for me. With my damaged brain already running with millions to billions less neurons I'll pass on more brain shrinkage. But I'm not medically trained so don't listen to me.

From this article comes the following paragraphs:

YIKES! FDA Approves Lecanemab Against Alzheimer’s

But there is a new and disturbing fly in the ointment.. A study published in the journal Neurology (March 27, 2023) reveals that anti-amyloid drugs like lecanemab can cause brain shrinkage. The researchers call this accelerated “brain atrophy.” 

Alzheimer’s Drug Reduces Amyloid but Fails to Restore Brain Waste Flow

Summary: Researchers found that lecanemab, the Alzheimer’s drug designed to clear amyloid-β plaques, does not improve the brain’s waste clearance system in the short term. In a three-month study using MRI-based DTI-ALPS imaging, scientists observed no measurable recovery in glymphatic function after treatment.

This suggests that once neuronal and clearance system damage occurs, it may be too advanced to reverse quickly. The results emphasize the need for multi-targeted strategies to address Alzheimer’s disease beyond amyloid reduction alone.

Key Facts

  • Study Finding: Lecanemab reduces amyloid-β but doesn’t restore glymphatic waste clearance after 3 months.
  • Implication: Short-term therapy may not repair established neuronal damage in Alzheimer’s.
  • Future Direction: Research will assess long-term effects and age-related factors influencing treatment outcomes.

Source: Osaka Metropolitan University

A group from Osaka Metropolitan University in Japan, led by graduate student Tatsushi Oura and Dr. Hiroyuki Tatekawa, found that treatment using the drug lecanemab to remove amyloid plaques in the brain does not change the waste clearance function in the brains of Alzheimer’s disease (AD) patients in the short term.

This suggests that even after treatment, the AD patients’ nerves are already damaged, and the waste clearance function does not recover in the short term. Their findings show the complexity of the disease and the need to address multiple disease-causing pathways simultaneously in the future.

Their findings add to the complicated process of unraveling AD’s mechanisms. Despite being the most common form of neurodegenerative disease, it is tricky to treat because of its multiple causes.

One cause of the nervous damage common in AD is the accumulation of the protein amyloid-β (Aβ) in the brain. In healthy patients, the glymphatic system moves cerebrospinal fluid along the spaces around the arteries into the brain tissue, where it mixes with interstitial fluid to carry away metabolic waste like Aβ. This is called the ‘glymphatic system’ after the glial cells involved in the process.

However, in AD patients, Aβ builds up, stiffening arteries and reducing the flow from the brain to the cerebrospinal fluid. This blockage triggers a chain of neurodegenerative processes, leading to AD symptoms.

The recently approved therapeutic lecanemab reduces accumulated Aβ. The team from the university’s Graduate School of Medicine evaluated the glymphatic system before and after treatment in patients who received lecanemab therapy, using the DTI-ALPS index.

Contrary to expectations, they found no significant change in the index between pre-treatment and 3 months after treatment.

They concluded that although anti-amyloid therapy can reduce plaque burden and slow further cognitive worsening, it may be insufficient to restore lost function. This suggests that neuronal damage and clearance system deficits have already been well established by the time the patient starts showing symptoms. Their findings show the range of factors involved in the progression of AD, many of which are not easily reversible.

“Even when Aβ is reduced by lecanemab, impairment of the glymphatic system may not recover within the short-term,” Oura said.

“In the future, we want to look at factors like age, the stage of the disease, and degree of lesions in the white matter to further understand the relationship between changes in the glymphatic system due to lecanemab treatment and the outcome of treatment. This will help understand the best way to administer treatment to patients.”

Funding: This study was supported by the Takeda Science Foundation (ROR ID: 02y123g31) and Japan Society for the Promotion of Science (JSPS) KAKENHI (grant number: 25K19115). Data were obtained from the OASIS (OASIS-3, Longitudinal Multimodal Neuroimaging: Principal Investigators: T. Benzinger, D. Marcus, and J. Morris, supported by NIH Grants: NIH P30 AG066444, P50 AG00561, P30 NS09857781, P01 AG026276, P01 AG003991, R01 AG043434, UL1 TR000448, and R01 EB009352).

Wednesday, November 19, 2025

Amyloid-clearing drug fails to change waste clearance function in the brains of Alzheimer's patients

 

Whoops, lecanemab is not for me. With my damaged brain already running with millions to billions less neurons I'll pass on more brain shrinkage. But I'm not medically trained so don't listen to me.

From this article comes the following paragraphs:

YIKES! FDA Approves Lecanemab Against Alzheimer’s

But there is a new and disturbing fly in the ointment.. A study published in the journal Neurology (March 27, 2023) reveals that anti-amyloid drugs like lecanemab can cause brain shrinkage. The researchers call this accelerated “brain atrophy.” 


Amyloid-clearing drug fails to change waste clearance function in the brains of Alzheimer's patients

A group from Osaka Metropolitan University in Japan, led by graduate student Tatsushi Oura and Dr. Hiroyuki Tatekawa, found that treatment using the drug lecanemab to remove amyloid plaques in the brain does not change the waste clearance function in the brains of Alzheimer's disease (AD) patients in the short term.

This suggests that even after treatment, the AD patients' nerves are already damaged, and the waste clearance function does not recover in the short term. Their findings show the complexity of the disease and the need to address multiple disease-causing pathways simultaneously in the future.

Their findings add to the complicated process of unraveling AD's mechanisms. Despite being the most common form of neurodegenerative disease, it is tricky to treat because of its multiple causes.

One cause of the nervous damage common in AD is the accumulation of the protein amyloid-β (Aβ) in the brain. In healthy patients, the glymphatic system moves cerebrospinal fluid along the spaces around the arteries into the brain tissue, where it mixes with interstitial fluid to carry away metabolic waste like Aβ. This is called the 'glymphatic system' after the glial cells involved in the process.

However, in AD patients, Aβ builds up, stiffening arteries and reducing the flow from the brain to the cerebrospinal fluid. This blockage triggers a chain of neurodegenerative processes, leading to AD symptoms.

The recently approved therapeutic lecanemab reduces accumulated Aβ. The team from the university's Graduate School of Medicine evaluated the glymphatic system before and after treatment in patients who received lecanemab therapy, using the DTI-ALPS index.

Contrary to expectations, they found no significant change in the index between pre-treatment and 3 months after treatment.

They concluded that although anti-amyloid therapy can reduce plaque burden and slow further cognitive worsening, it may be insufficient to restore lost function. This suggests that neuronal damage and clearance system deficits have already been well established by the time the patient starts showing symptoms. Their findings show the range of factors involved in the progression of AD, many of which are not easily reversible.

Even when Aβ is reduced by lecanemab, impairment of the glymphatic system may not recover within the short-term. In the future, we want to look at factors like age, the stage of the disease, and degree of lesions in the white matter to further understand the relationship between changes in the glymphatic system due to lecanemab treatment and the outcome of treatment. This will help understand the best way to administer treatment to patients."

Tatsushi Oura, graduate student, Osaka Metropolitan University

The study was published in Journal of Magnetic Resonance Imaging.

Source:
Journal reference:

Oura, T., et al. (2025). Unchanged Early Diffusion Tensor Imaging Along Perivascular Space Index After Amyloid‐Targeting Disease‐Modifying Therapy in Alzheimer’s Disease: A Preliminary Study. Journal of Magnetic Resonance Imaging. doi: 10.1002/jmri.70118. https://onlinelibrary.wiley.com/doi/10.1002/jmri.70118

Thursday, October 23, 2025

Heavy drinking fuels Alzheimer’s disease by igniting brain inflammation and protein damage

I'm using bar nights of jazz(Sunday and Tuesday) and trivia(Thursday) to vastly expand my social connections which is what is going to prevent dementia and this includes alcohol. You can't listen to me; I'm not medically trained. Better stroke recovery from music and better cognition from trivia; so there.

There May Be No Safe Amount of Booze When It Comes to Dementia Risk

 I completely disagree!


Alcohol use disorder (AUD) is defined as a problematic pattern of alcohol use leading to significant impairment or distress, marked by an inability to stop or control drinking despite negative consequences. Not applicable to me.

The latest here:

Heavy drinking fuels Alzheimer’s disease by igniting brain inflammation and protein damage

A new review uncovers how chronic alcohol consumption accelerates Alzheimer’s pathology through oxidative stress and neuroinflammatory cascades, while spotlighting promising molecular and metabolic interventions to protect the brain.

Review: Alcohol addiction and Alzheimer’s disease: a molecular collision course. Image Credit: Antonio Marca / Shutterstock

Review: Alcohol addiction and Alzheimer’s disease: a molecular collision course. Image Credit: Antonio Marca / Shutterstock

In a recent article published in the journal Translational Psychiatry, researchers reviewed the contribution of chronic alcohol consumption to AD, focusing on its damage to neural pathways, disruption of neurotransmitters, and intensification of oxidative stress and inflammation. The review clarifies that “AUD” is the preferred diagnostic term, while “alcohol addiction” refers to severe AUD characterized by compulsive use and loss of control.

The current evidence suggests that excessive use of alcohol heightens vulnerability to AD through multiple molecular mechanisms, but that personalized treatments, early interventions, and neuroprotective drugs could slow the progression of the disease and reduce risk.

Alcohol consumption and Alzheimer’s

Alcohol use disorder (AUD) and AD are major causes of cognitive decline with overlapping brain, molecular, and behavioral abnormalities. AUD ranges from mild to severe forms of dependence characterized by craving, loss of control, and continued drinking despite harm.

Both AD and AUD affect similar brain regions, especially the prefrontal cortex and hippocampal-limbic circuitry, leading to impairments in executive function, decision-making, and behavior regulation. Epidemiological studies increasingly show that AUD is an independent risk factor for AD and AD-like dementia.

Both disorders disrupt large-scale brain networks such as the default mode network and share symptoms like emotional instability and sleep disturbances. At the molecular level, prolonged alcohol exposure accelerates AD-related changes, including amyloid-beta buildup, tau phosphorylation, and chronic neuroinflammation.

Experimental findings reveal complex, dose-dependent effects, with low alcohol exposure occasionally showing model-specific signals of neuroprotection in preclinical studies, but chronic heavy drinking causing severe neurotoxicity. As neuroinflammation and metabolic dysregulation are key shared mechanisms linking the two diseases, a deeper understanding of how alcohol addiction intensifies AD pathology could guide strategies for targeted prevention. Sex may also modulate these effects, influencing microglial responses and neuroinflammatory severity.

Underlying mechanisms

Alcohol contributes to AD through multiple interconnected mechanisms that damage brain cells and disrupt molecular signaling.

Chronic alcohol exposure increases oxidative stress by generating excess reactive oxygen species (ROS) and overwhelming antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx), which damages mitochondria and impairs cellular energy production in the hippocampus, a region vital for memory. These effects lead to neuronal death, disrupted calcium regulation, and impaired neuroplasticity.

Alcohol also activates inflammatory pathways such as TLR4/NF-κB and suppresses antioxidant defenses (Nrf2/HO-1), creating a feedback loop of inflammation and oxidative damage.

Additionally, alcohol suppresses hippocampal neurogenesis by triggering neuroinflammation, disrupting the balance of cholinergic and glutamatergic signaling, and activating cannabinoid receptors that promote neuronal apoptosis.

It alters neurotransmitter systems, reducing acetylcholine synthesis, disturbing gamma-aminobutyric acid (GABA)/glutamate balance, and impairing dopamine and serotonin regulation, causing cognitive and emotional disturbances typical of both AUD and AD.

Neuroinflammation is further intensified by microglial M1 polarization and astrocyte activation, leading to chronic inflammation and neuronal loss.

At the molecular level, ethanol promotes tau hyperphosphorylation via GSK-3β and JNK pathways and increases amyloid-beta () accumulation by enhancing BACE1 activity and reducing  clearance through impaired insulin-degrading enzyme (IDE) and low-density lipoprotein receptor-related protein 1 (LRP1). These combined effects accelerate AD-like neurodegeneration, with dose, duration, and sex influencing severity.

Counteracting AUD-AD links

Several emerging therapeutic strategies aim to counteract the biological links between alcohol addiction and AD. Targeting key molecular pathways, dual inhibition of p38 MAPK and GSK-3β has shown promise in reducing tau hyperphosphorylation, amyloid formation, and oxidative stress.

Compounds such as MW150, sanggenon C, and magnesium improve memory and neuronal survival, while nanodrug delivery and structural optimization may enhance their brain bioavailability.

TLR4 antagonists, including TAK-242 and novel derivatives of tanshinone IIA and dihydroartemisinin, suppress neuroinflammation by blocking NF-κB and MAPK signaling, although translation is limited by blood–brain barrier penetration and pharmacokinetic constraints (for example, the clinical failure of Eritoran underscores these challenges).

Neurotransmitter-targeted treatments aim to restore cholinergic-GABAergic balance and glutamate regulation. Co-modulators and drugs like riluzole show potential for improving cognition and synaptic stability.

Metabolic interventions focus on enhancing acetaldehyde clearance via ALDH2 activation using compounds such as Alda-1, and selective use of probiotics; for example, Duolac ProAP4 lowered blood acetaldehyde only in ALDH2*2 carriers, with no effect in wild-type individuals.

Epigenetic therapies using histone deacetylase (HDAC) inhibitors (such as vorinostat or sodium butyrate) restore histone acetylation and synaptic plasticity, mitigating alcohol-induced oxidative stress.

Addressing brain insulin resistance with antioxidants and nutrients such as ω-3 fatty acids, curcumin, and vitamin D is an area of active investigation, with mixed and preliminary clinical evidence and a need for better-designed trials, which may slow AD progression if future studies confirm benefit.

Finally, early abstinence combined with cognitive training strengthens neuroplasticity, while personalized nutritional strategies integrating genetics and metabolism offer a path toward precision therapy in alcohol-related AD prevention.

Conclusions

Current evidence indicates that alcohol addiction accelerates AD progression through shared molecular mechanisms involving oxidative stress, neuroinflammation, and microglial activation.

Chronic alcohol exposure heightens ROS production and promotes pro-inflammatory M1 microglial polarization, contributing to neuronal damage. A major challenge for therapeutic advancement is poor blood–brain barrier permeability, which limits drug delivery. Nanotechnology-based approaches such as lipid-polymer hybrids, chitosan-hyaluronic acid nanoparticles, and gold nanorods show promise in enhancing brain drug accumulation, detecting and inhibiting  aggregation, and restoring neuronal function.

Future research should focus on optimizing dual-functional nanoparticles targeting key signaling pathways, improving blood–brain barrier transport, and validating safety thresholds for nanomaterials.

Developing biomarker models using p-tau217 and neurofilament light chains may help identify high-risk individuals with AUD. Advanced tools like organoid models and in vivo imaging will be essential to clarify alcohol–AD interactions and guide precision, safe therapeutic development.

Journal reference:
  • Chang, J.-S., Huang, H.-Z., Yuan, M., Zhou, Y., Liu, D., Zhan, K.-B., Zhu, L.-Q. (2025). Alcohol addiction and Alzheimer’s disease: a molecular collision course. Translational Psychiatry 15, 410. DOI: 10.1038/s41398-025-03619-6, https://www.nature.com/articles/s41398-025-03619-6


Wednesday, October 22, 2025

Scientists Studied 'SuperAgers' For 25 Years And Found That They All Have This 1 Habit In Common

 

I'm using bar nights of jazz(Sunday and Tuesday) and trivia(Thursday) to vastly expand my social connections which is what is going to prevent dementia and this includes alcohol. You can't listen to me; I'm not medically trained. Better stroke recovery from music and better cognition from trivia; so there.

There May Be No Safe Amount of Booze When It Comes to Dementia Risk

 I completely disagree!

The latest here:

Scientists Studied 'SuperAgers' For 25 Years And Found That They All Have This 1 Habit In Common

  • Northwestern University is conducting ongoing research into SuperAgers and just released a new study published in Alzheimer's & Dementia based on 25 years of data collection.
  • SuperAgers are individuals 80+ with cognitive function that's on part with a middle-aged person.
  • The SuperAgers had one interesting characteristic in common, which was related to their social life.

In a perfect world, we'd all stay mentally sharp until the very end. Unfortunately, that tends to be the exception rather than the norm. But ongoing research following the health habits of older adults with exceptional cognitive health has found some really interesting takeaways the rest of us can steal.These so-called "SuperAgers" are 80 or older, with cognitive function that’s on par with an average person who is middle-aged. (Think: An 85-year-old with a 55-year-old's brain function.) They also have less brain volume loss than is typical for someone of their age, and seem to be better protected from developing dementia compared to their peers.

Naturally, researchers want to study them, and Northwestern University has ongoing research that tracks these SuperAgers—and they just released findings after 25 years of studying these medical phenoms....

Meet the experts: Clifford Segil, DO, is a neurologist at Providence Saint John’s Health Center in Santa Monica, CA; Scott Kaiser, MD, is a geriatrician and Director of Geriatric Cognitive Health for the Pacific Neuroscience Institute

What exactly did the study find?

The scientific perspective paper, which was published in the journal Alzheimer’s & Dementia, is part of ongoing research into said SuperAgers. It notes a lot of interesting factors, like that SuperAgers have less brain thinning as they get older compared to other people of the same age, and that they have less Alzheimer's disease–type changes in the brain. As the research is still ongoing, scientists aren’t exactly sure why this is the case.

Related video: These Personality Traits Are Linked to a Longer Life, Experts Say (The Hearty Soul)

But the researchers also discovered that SuperAgers tend to share certain lifestyle and personality traits. A key one worth noting: These older adults tend to be highly social and outgoing. (We can get on board with that!)

Why does socializing help your memory as you age?

There are a few possible things going on here. The researchers found that SuperAgers have more than four to five times the number of large, spindly neurons called von Economo neurons in their brains, which are thought to play a role in social processing and awareness. (It’s just not clear if being socially active causes this or if you tend to socialize more when you have more of these neurons in your brain to begin with.)

But there is a growing push for people to stay social as they age for health reasons. “Chronic isolation can be as bad for your health as smoking,” says Scott Kaiser, MD, a geriatrician and Director of Geriatric Cognitive Health for the Pacific Neuroscience Institute. “Conversely, we know that healthy social connections are critical for improved cardiovascular health, neurological health, and reducing your risk of dementia.”Staying social lowers overall stress levels and increases levels of the feel-good hormone oxytocin, Kaiser points out. He also notes that people who feel well connected to others may be more likely to make healthy choices around their diet, drinking, and lifestyle—and that could support good physical and mental health even more.

But socializing also just works your brain, especially when you’re communicating with several people at once, says Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA. “The brain pathways required to juggle an interaction with multiple people is more complex and requires more processing space than a one-on-one interaction,” he says. Basically, being socially active is a workout for your brain.

Other ways to protect your brain as you age

Segil recommends doing a few things to protect your brain health as you get older. “I continuously advise my aging patients that structure is beneficial for the brain,” he says. “I advise people to take classes as they age.” Joining clubs, volunteering to help others, listening to music, and reading books can put your brain to work, too, he says.

But Segil also stresses the importance of being social as much as possible. “There are only potential benefits from being more social as you age,” he says.