Whole-Plant Extract Outperforms THC on Glycemia

 You obviously can't do this until 50 years from now when your doctor has a brain transplant and gets human testing going!

Whole-Plant Extract Outperforms THC on Glycemia

Regular cannabis users have long shown lower rates of obesity and type 2 diabetes despite the appetite-boosting "munchies" effect, a paradox that a new mouse study helps explain. Whole-plant cannabis extract improved glucose control and fat-pancreas signaling more than THC alone in obese, hyperglycemic mice. The data are preclinical and don't support cannabis use for weight or metabolic health.

1. A Curious Metabolic Signal

Cannabis triggers the “munchies”, yet regular users show lower rates of obesity and type 2 diabetes. The mouse study published in The Journal of Physiology points to a possible mechanism: disrupted "cross talk" between fat tissue and the pancreas, suggesting nonpsychoactive plant compounds, not delta-9-tetrahydrocannabinol (THC), may be doing the metabolic work.

2. Whole-Plant Outperforms THC Alone

Obese, hyperglycemic mice received either pure THC or a whole-plant extract, both dosed at 5 mg/kg THC to mimic blood levels after smoking cannabis. Both groups lost weight and fat, but only the extract group showed meaningfully better glucose regulation, glucose clearance approaching lean-mouse levels, and normalized adipokine activity. Per the study author, extract-treated mice showed reversal of type 2 diabetes markers that THC alone didn't match.

3. A Possible Fix for the Adipoinsular Axis

In obesity, signaling between fat cells and the pancreas, known as the adipoinsular axis, breaks down, driving blood sugar up. Cannabis compounds may help restore that communication line. The study author suspects CB1 receptors, present in the central nervous system, fat tissue, liver, and pancreas, are involved, though the exact mechanism is still unmapped.

4. Why the Munchies Fade

Acute THC activates CB1 receptors, boosting appetite and impairing short-term glucose tolerance. With repeated exposure, CB1 signaling downregulates, and effects often flip. Intake drops, and at the extreme end, chronic heavy use can produce cannabis hyperemesis syndrome.

5. What to Tell Patients

Further preclinical work is needed before this moves to human trials. Don't recommend recreational cannabis for weight or glycemic control. If patients ask about cannabis-based therapies, the message worth giving is that the target is the endocannabinoid receptor system itself, not cannabis use, and that long-term cardiometabolic risk with chronic use and aging still isn't well understood.

BOTTOM LINE:

In obese mice, whole-plant extract improved glycemic control and adipokine activity more than THC alone, likely by restoring fat-pancreas signaling. This finding does not support recommending cannabis for weight loss or diabetes management today. If patients ask, clinicians should clarify that the therapeutic target is the receptor system, not cannabis itself. They should also specify that human trials and long-term cardiometabolic risk remain unresolved.

This article is based on a recent Medscape article titled " How Cannabis Compounds May Help Create Weight-Loss Drugs" and was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Early statin therapy may lower risk for dementia in people with diabetes

 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: 

Early statin therapy may lower risk for dementia in people with diabetes

Key takeaways:

• Statin initiation after diagnosis of diabetes may lower risk for developing dementia vs. no statin initiation.
• Treating CV risk factors may also prevent cognitive decline in people with diabetes.

MUNICH — Statin initiation after a diagnosis of type 2 diabetes was associated with lower absolute and relative risk for all-cause dementia compared with no statin initiation, a speaker reported.

The effect was most pronounced in patients who initiated statin therapy within 1 year of their type 2 diabetes diagnosis, according to the researchers.

Data derived from Ternhamar T, et al. Diabetes and the heart: Pharmacotherapy. Presented at: European Society of Cardiology Congress; Aug. 28-31, 2026; Munich. 

Addressing traditional CV risk factors could also prevent development of dementia among people with diabetes, according to data presented at the European Society of Cardiology Congress and simultaneously published in The Lancet Regional Health – Europe.

“As we become better at treating some of the main killers, like heart disease, cancers and infectious diseases, we are seeing a progressively aging population, globally. We all see a large burden of dementia, especially in diabetes. As we don’t have any cure for dementia, attention has turned toward preventing it by targeting some of the cardiovascular risk factors that we see. Diabetes and elevated low-density lipoprotein cholesterol have been highlighted as two such risk factors,” Tummas Ternhamar, MD, clinical researcher at Copenhagen University Hospital and University of Copenhagen, Denmark, said during a presentation. “What we wanted to test was the hypothesis that early statin treatment at the point when a type 2 diabetes diagnosis is made is associated with lower risk of dementia [compared with] delayed initiation.”

Ternhamar and colleagues used nationwide registry data gathered from 2006 to 2019 to identify 132,585 individuals with a diagnosis of type 2 diabetes who were statin-naive. Participants were sorted into one of three categories: no statin initiation within 5 years after diabetes diagnosis; early statin initiation within 1 year of diagnosis; and late statin initiation at 1 to 5 years after diabetes diagnosis.

Participants were followed for a median of 7.1 years, and the primary outcome was 10-year risk for all-cause dementia, with death treated as a competing risk.

The researchers estimated that the 10-year absolute risk for dementia was 3.9% among patients who did not initiate a statin after diabetes diagnosis; 3.3% among those who initiated early; and 3.5% among those who initiated late after diabetes diagnosis.

Compared with no statin initiation, early statin treatment was associated with a 15% lower 10-year relative risk for dementia (95% CI, 9%-21%) and late statin initiation was associated with a 10% lower 10-year relative risk for dementia (95% CI, 3%-15%), according to the study.

The researchers estimated that early statin initiation after diabetes diagnosis was associated with an absolute risk difference of 0.59% (95% CI, 0.34%-0.86%) while late statin initiation was associated with a 0.38% absolute risk difference (95% CI, 0.12%-0.61%) compared with no statin initiation.

“In statin-naive individuals who developed diabetes, statin therapy was associated with a lower relative and absolute risk of dementia, which was most pronounced in those with early statin initiation,” Ternhamar said during the presentation. “It highlights potential for targeting some of the traditional cardiovascular risk factors, LDL cholesterol in this case, for improving brain health and dementia risk.”

Three Factors Tied to 13 Additional Dementia-Free Years

 Never smoked, hypertension started at age 58(past midlife), no diabetes or pre-diabetes. I should easily get to 100 without dementia(30 years to go).

Three Factors Tied to 13 Additionedal Dementia-Free Years

Key Takeaways

• Midlife vascular health was associated with nearly 13 more dementia-free years in a prospective U.S. cohort study.
• At age 55, healthier study participants averaged 30.1 additional years without dementia.
• Smoking, hypertension, and diabetes together sharply increased dementia risk and mortality.

Maintaining three key health factors during midlife -- normal blood pressure, no diabetes, and not smoking -- was associated with nearly 13 additional dementia-free years, a study of 12,000 people in the U.S. showed.

Individuals who met these criteria at age 55 lived an average 30.1 more years dementia-free, reported Josef Coresh, MD, PhD, of NYU Langone Health in New York City, and co-authors.

Conversely, those who smoked, had hypertension, and had diabetes at age 55 had dementia-free survival of only 17.5 years, Coresh and colleagues wrote in Neurology Open Access.

People with all three risk factors had a higher incidence of dementia (HR 2.69, 95% CI 1.94-3.73) and a higher incidence of dying before a dementia diagnosis (HR 5.61, 95% CI 4.67-6.74) compared with those who had no risk factors.

Overall, women lived longer without dementia than men at all risk levels. White participants had more years free of dementia than Black participants, and APOE4 carriers had shorter dementia-free survival than noncarriers.

"Our findings argue that people need to actively avert these factors in midlife as a strategy for preserving brain health for more than a decade," Coresh said in a statement. "Discovering new ways to delay dementia is crucial with 42% of Americans at risk for developing the condition at any time after age 55."

The findings were based on 12,409 participants in the prospective Atherosclerosis Risk in Communities (ARIC) study, which started in 1986 to evaluate midlife vascular risk factors and late-life dementia.

Previous research from the ARIC cohort suggested that 22% to 44% of dementia risk by age 80 could be attributed to three vascular risk factors measured in midlife and early late life, after accounting for risk factor concurrence and interactions.

Hypertension was defined as systolic blood pressure ≥130 mm Hg, diastolic blood pressure ≥80 mm Hg, or the use of blood pressure medication; diabetes as fasting glucose ≥126 mg/dL, non-fasting glucose ≥200 mg/dL, a physician's diagnosis, or the use of any diabetes medication; and current smoking was self-reported.

"Our study complements this important work by shifting focus from probability-based and attributable risk metrics to a time-based estimand -- dementia-free survival years, which quantifies the expected duration of life lived cognitively intact," Coresh and colleagues wrote.

"This outcome integrates two clinically relevant processes: incident dementia and death before dementia, therefore reflecting the competing risks that shape real-world aging trajectories," they pointed out. "In contrast to previous ARIC studies, this framework emphasizes how vascular health influences the balance between longevity and cognitive health over the life course."

In the current analysis, ARIC participants had a mean baseline age of 56 and 56% were women. Dementia was tracked through cognitive assessments, informant interviews, and continuous surveillance. Deaths without dementia were captured from multiple sources including the National Death Index.

Over a median follow-up of 26.3 years, 3,008 cases of dementia and 5,238 deaths without dementia were documented. Better vascular health was linked with longer dementia-free survival in a dose-response pattern.

"Several biologic pathways likely underlie our observed associations between vascular health and dementia-free survival, including chronic cerebrovascular injury, neuroinflammation triggered by vascular damages through hypertension and diabetes, and cumulative oxidative stress resulting from smoking," Coresh and colleagues wrote. "Together, these factors likely accelerate atherosclerosis, increase stroke risk, and may facilitate Alzheimer's disease pathology through promoting amyloid plaques and tau tangles."

The findings relied on one midlife assessment of risk factors, the researchers acknowledged. Dementia ascertainment may have differed between participants who attended recent visits and those who didn't. In addition, the study was observational and residual confounding may have influenced outcomes.

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Scientists reveal 3 lifestyle factors that may delay dementia by 12 years

 Not defined is whether high blood pressure being treated is still a risk factor, like me.

Scientists reveal 3 lifestyle factors that may delay dementia by 12 years

According to the National Institutes of Health (NIH), about 42% of Americans over the age of 55 will develop dementia at some point. Luckily, a growing body of research suggests there are concrete steps you can take to reduce your risk or delay the disease’s onset.

Most recently, a study in Neurology found that just three lifestyle factors may add up to 12 dementia-free years to your life. For the study, the researchers observed more than 12,000 participants over an average of 26 years, investigating how three vascular risk factors—diabetes, high blood pressure, and smoking status—affected their risk of developing dementia and its age of onset. Ultimately, the researchers found that people who had fewer of these risk factors at midlife were both less likely to develop dementia and less likely to develop dementia at an early age. In fact, compared to participants with all three risk factors, participants with no risk factors had about 12.6 additional dementia-free years. (Participants with just one risk factor also had 8.8 more dementia-free years, while participants with two risk factors had 3.5.)

“This builds beautifully on an important 2024 Lancet Commission report, which identified 14 potentially modifiable risk factors for dementia. Diabetes, hypertension, and smoking are only part of that much larger picture,” says David Perlmutter, M.D., F.A.C.N., A.B.I.H.M., board-certified neurologist and author of Brain Defenders. “The message from both reports is increasingly difficult to ignore: a meaningful portion of dementia risk is related to factors we can potentially influence.”

So, what does all this mean for you? Ahead, neurologists break it down.

Meet the experts: David Perlmutter, M.D., F.A.C.N., A.B.I.H.M., board-certified neurologist and author of Brain Defenders; Jeremy M. Liff, M.D., board-certified neurologist in New York City

Why are the findings significant?

The importance of the study’s findings is twofold. First, “they reinforce the idea that dementia is significantly preventable,” Dr. Perlmutter says. “To me, the important message is that brain health is very much connected to metabolic and vascular health, and what happens in midlife can have profound consequences decades later.” This is particularly important because we don’t yet have good treatments for dementia or Alzheimer’s disease, he notes.

Related video: Nearly half of dementia cases may be preventable, doctor explains (FOX 32 Chicago) Second, the results show that the risk factors appear to be additive. “One risk factor is concerning; two are worse; and three are considerably worse,” Dr. Perlmutter says. “People with all three had about 2.7 times the hazard of developing dementia compared with those who had none.”

What’s the takeaway?

While there’s no way to completely eliminate the risk that you’ll develop dementia—and preventing or delaying the onset of diabetes or hypertension is a complex, multifactorial process as well—the study shows that you can take some important steps to reduce your dementia risk.

“Threats to brain health begin long before memory problems appear. Know your blood pressure. Know your blood sugar and metabolic health. Don’t smoke,” Dr. Perlmutter says. “These aren’t exotic, expensive, or difficult interventions, and that’s precisely the point. Many of the most powerful tools we have for protecting the aging brain are available to each of us right now... This fundamentally changes the conversation from simply asking, ‘How can we treat Alzheimer’s?’ to asking, ‘How can we reduce the likelihood of getting there in the first place?’”

Taking these steps won’t just affect your dementia risk, either. “Smoking, diabetes, and blood pressure are clearly risk factors that would stop you from living a longer, generally healthier life—not just brain health, but overall body health,” says Jeremy M. Liff, M.D., board-certified neurologist based in New York City.

And it’s never too early to make healthy changes. “Don’t wait until you’re in your mid-70s,” Dr. Liff urges. “One of the points of the study is they were looking at people in their 50s, so the time to start with this is now, because what you do now will have that downstream effect 20 to 40 years from now.”

Dr. Perlmutter agrees. “This fits perfectly with what we’re learning about Alzheimer’s disease. The biological changes that ultimately manifest as memory loss may be developing for 20 or even 30 years before the diagnosis,” he explains. “I think we’ve made a mistake by viewing Alzheimer’s simply as a disease of old age. Increasingly, we should think about it as a disease whose foundations may be laid in midlife or even earlier.”

How can you support your brain health?

Again, there’s no surefire way to avoid developing dementia or Alzheimer’s disease; as Dr. Liff notes, there are plenty of otherwise healthy patients who still develop it.

Still, there are things you can do to support your brain health throughout your life. “I encourage people to think beyond any single supplement, food, drug, or ‘brain hack.’ Brain health reflects what we do consistently over many years,” Dr. Perlmutter says.

In addition to monitoring your risk of developing diabetes or hypertension, and refraining from smoking, both Dr. Liff and Dr. Perlmutter recommend the following habits for good brain health:

• Get regular exercise
• Prioritize restorative sleep
• Maintain meaningful social connections
• Eat a minimally-processed diet rich in fiber and whole foods
• Continue learning and challenging yourself
• Protect your hearing
• Avoid large amounts of alcohol
• Avoid stimulants late at night

The bottom line

This study and others like it suggest we have more control over our dementia risk than we previously thought, but it’s important to keep these findings in context. Both Dr. Liff and Dr. Perlmutter point out that the research is observational, which means that while the studies found a clear association between vascular risk factors and dementia risk, they can’t establish a cause-and-effect relationship. Additionally, the researchers only assessed the participants for diabetes, hypertension, and smoking status at one point in midlife, rather than tracking the evolution of these risk factors over a longer period of time.

“And, of course, dementia is complicated. Genetics, environmental exposures, education, physical activity, social circumstances, and many other factors matter as well,” Dr. Perlmutter adds. “But again, many of these other factors reflect our lifestyle choices. And that gives each of us agency over our brain’s destiny.”

Three Factors Tied to 13 Additional Dementia-Free Years

 Ask your competent? doctor how your stroke affects these possibilities! There better be an answer.

Three Factors Tied to 13 Additional Dementia-Free Years

Key Takeaways

• Midlife vascular health was associated with nearly 13 more dementia-free years in a prospective U.S. cohort study.
• At age 55, healthier study participants averaged 30.1 additional years without dementia.
• Smoking, hypertension, and diabetes together sharply increased dementia risk and mortality.

Maintaining three key health factors during midlife -- normal blood pressure, no diabetes, and not smoking -- was associated with nearly 13 additional dementia-free years, a study of 12,000 people in the U.S. showed.

Individuals who met these criteria at age 55 lived an average 30.1 more years dementia-free, reported Josef Coresh, MD, PhD, of NYU Langone Health in New York City, and co-authors.

Conversely, those who smoked, had hypertension, and had diabetes at age 55 had dementia-free survival of only 17.5 years, Coresh and colleagues wrote in Neurology Open Access.

People with all three risk factors had a higher incidence of dementia (HR 2.69, 95% CI 1.94-3.73) and a higher incidence of dying before a dementia diagnosis (HR 5.61, 95% CI 4.67-6.74) compared with those who had no risk factors.

Overall, women lived longer without dementia than men at all risk levels. White participants had more years free of dementia than Black participants, and APOE4 carriers had shorter dementia-free survival than noncarriers.

"Our findings argue that people need to actively avert these factors in midlife as a strategy for preserving brain health for more than a decade," Coresh said in a statement. "Discovering new ways to delay dementia is crucial with 42% of Americans at risk for developing the condition at any time after age 55."

The findings were based on 12,409 participants in the prospective Atherosclerosis Risk in Communities (ARIC) study, which started in 1986 to evaluate midlife vascular risk factors and late-life dementia.

Previous research from the ARIC cohort suggested that 22% to 44% of dementia risk by age 80 could be attributed to three vascular risk factors measured in midlife and early late life, after accounting for risk factor concurrence and interactions.

Hypertension was defined as systolic blood pressure ≥130 mm Hg, diastolic blood pressure ≥80 mm Hg, or the use of blood pressure medication; diabetes as fasting glucose ≥126 mg/dL, non-fasting glucose ≥200 mg/dL, a physician's diagnosis, or the use of any diabetes medication; and current smoking was self-reported.

"Our study complements this important work by shifting focus from probability-based and attributable risk metrics to a time-based estimand -- dementia-free survival years, which quantifies the expected duration of life lived cognitively intact," Coresh and colleagues wrote.

"This outcome integrates two clinically relevant processes: incident dementia and death before dementia, therefore reflecting the competing risks that shape real-world aging trajectories," they pointed out. "In contrast to previous ARIC studies, this framework emphasizes how vascular health influences the balance between longevity and cognitive health over the life course."

In the current analysis, ARIC participants had a mean baseline age of 56 and 56% were women. Dementia was tracked through cognitive assessments, informant interviews, and continuous surveillance. Deaths without dementia were captured from multiple sources including the National Death Index.

Over a median follow-up of 26.3 years, 3,008 cases of dementia and 5,238 deaths without dementia were documented. Better vascular health was linked with longer dementia-free survival in a dose-response pattern.

"Several biologic pathways likely underlie our observed associations between vascular health and dementia-free survival, including chronic cerebrovascular injury, neuroinflammation triggered by vascular damages through hypertension and diabetes, and cumulative oxidative stress resulting from smoking," Coresh and colleagues wrote. "Together, these factors likely accelerate atherosclerosis, increase stroke risk, and may facilitate Alzheimer's disease pathology through promoting amyloid plaques and tau tangles."

The findings relied on one midlife assessment of risk factors, the researchers acknowledged. Dementia ascertainment may have differed between participants who attended recent visits and those who didn't. In addition, the study was observational and residual confounding may have influenced outcomes.

Midlife Vascular Health Adds Nearly 13 Dementia-Free Years

 My blood pressure didn't spike until age 60, now controlled, the rest I'm good at. But ask your competent? doctor if your stroke negates these factors! NO answer; PURE FUCKING INCOMPETENCE!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Midlife Vascular Health Adds Nearly 13 Dementia-Free Years

Summary: Maintaining healthy blood pressure, avoiding diabetes, and not smoking between ages 48 and 68 is associated with nearly 13 additional years of dementia-free life.

While the presence of all three vascular risk factors significantly accelerated dementia onset and reduced dementia-free survival across all groups, the researchers noted key demographic variations: women lived longer without dementia than men regardless of risk profile, and white participants experienced longer dementia-free lifespans than Black participants under similar risk conditions.

Key Facts

• 13-Year Healthspan Gain: Individuals free of hypertension, diabetes, and smoking from ages 48 to 68 lived an average of nearly 13 additional years without developing dementia compared to those with all three risk factors (30 years vs. 17 years post-baseline).
• Broad Cohort Scope: Analyzed 12,409 participants (average baseline age of 56) followed over a 26-year tracking period, during which 3,008 developed dementia and 5,238 died dementia-free.
• Sex-Based Differences: Women consistently maintained longer dementia-free survival than men across equivalent risk categories (18.1 years for women with all three risk factors vs. 16.6 years for men).
• Racial Disparities: White participants with all three risk factors lived an average of 19.6 dementia-free years compared to 16.0 years for Black participants, emphasizing the need for targeted midlife interventions in vulnerable populations.
• Critical Prevention Window: Emphasizes age 48 to 68 as a crucial developmental window where aggressive vascular risk modification directly safeguards cognitive reserve in later life.

Source: NYU

Having normal blood pressure, no diabetes, and not smoking from age 48 to 68, are associated with nearly 13 additional years on average of dementia-free life, a new study shows.

Led by NYU Langone Health researchers, the new work also found that, no matter how many risk factors they had, women lived longer without dementia than men, and that white study participants had more dementia-free years than Black participants.

Avoiding midlife vascular risk factors adds nearly 13 additional years of dementia-free life. Credit: Neuroscience News

Published online Aug. 5 in Neurology, the study results underscore the dual impact of the identified midlife risk factors, the presence of which was linked to both accelerated dementia onset and shortened overall dementia-free lifespans.

“Our findings argue that people need to actively avert these factors in midlife as a strategy for preserving brain health for more than a decade,” said study senior investigator Josef Coresh, MD, PhD, founding director, Optimal Aging Institute, NYU Langone.

“Discovering new ways to delay dementia is crucial with 42 percent of Americans at risk for developing the condition at any time after age 55.” Dr. Coresh is also the Terry and Mel Karmazin Professor, Department of Population Health, NYU Langone.

For the new study, the researchers analyzed data in the community-based Atherosclerosis Risk in Communities (ARIC) Study, which started in 1986 and followed participants over decades into late life, measuring midlife vascular risk factors and dementia.

The current study looked at 12,409 people with an average age of 56 who were free of dementia. Participants were assessed for three risk factors: high blood pressure, diabetes, and smoking. They were then followed for an average of 26 years. During that time, 3,008 developed dementia and 5,238 people died without developing dementia. Those who had no risk factors lived without developing dementia nearly 13 years longer than people with the three risk factors (30 years total after the study’s start versus 17 years).

The team also sought to determine how cardiovascular risk factors in midlife influenced dementia-free survival across demographics. Women with all three risk factors lived an average of 18.1 years from the start of tracking without developing dementia, compared to 16.6 years for male study participants. White participants with all three risk factors lived an average of 19.6 years without developing dementia, compared to 16 years for Black participants.

“These results suggest that vascular risk reduction may benefit all groups, but that certain populations, such as Black adults, may especially benefit from targeted prevention efforts,” Dr. Coresh added. “Hopefully, these results will encourage people to stop smoking and watch their vascular health closely from age 48 on.”

Importantly, the study was not designed to prove that avoiding these vascular risk factors caused the observed delay in dementia — only that they were associated with each other. Another limitation of the study was that the risk factor measurement was performed just once, so changes over time were not captured.

Funding: This study was supported by National Institutes of Health (NIH) grants K24HL152440 and K01DK138273, and the ARIC study was funded by grants NIH U01HL096812, U01HL096814, U01HL096899, U01HL096902 and U01HL096917.

Along with Dr. Coresh, study authors are Jiaqi Hu, Institute for Hospital Management, Tsinghua University in Beijing (lead author); Jason Smith, University of North Carolina School of Medicine; A. Richey Sharrett, Elizabeth Selvin and Michael Fang, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health; Rebecca F. Gottesman, Stroke Branch, National Institute of Neurological Disorders and Stroke; Pamela Lutsey, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota; Thomas H. Mosley Jr., MIND Center, University of Mississippi Medical Center School of Medicine, Jackson; and Jordan Weiss, Department of Medicine (Division of Precision Medicine) and Optimal Aging Institute, NYU Grossman School of Medicine.

Key Questions Answered:

Q: Why are midlife vascular factors so influential on dementia risk decades later?

A: Midlife hypertension, diabetes, and smoking cause cumulative structural damage to the brain’s microvasculature. Chronic hypoperfusion, small vessel disease, inflammation, and blood-brain barrier breakdown reduce cognitive resilience and accelerate pathological protein accumulation, laying the groundwork for clinical dementia late in life.

Q: What did the study reveal regarding health disparities between demographic groups?

A: Even when carrying the same three vascular risk factors, Black participants experienced shorter dementia-free lifespans (16.0 years) than white participants (19.6 years). This highlights that systemic healthcare disparities, social determinants of health, and differences in baseline disease severity likely amplify the cognitive burden of vascular risk in Black communities.

Q: Did the study establish that treating these risk factors directly prevents dementia?

A: The study demonstrated a strong prospective association rather than direct causation. Because risk factors were measured at baseline, the observational design does not capture how midlife treatment changes over time impact dementia trajectories, though the robust 26-year tracking strongly supports midlife risk reduction as a primary preventative strategy.

Editorial Notes:

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

About this dementia and aging research news

Author: David March
Source: NYU
Contact: David March – NYU
Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Neurology

Newly discovered coffee compounds beat diabetes drug in lab tests

 More reasons for my 12 cup pot of coffee a day. Don't follow me, I'm not medically trained.

coffee (384 posts to February 2012)

Newly discovered coffee compounds beat diabetes drug in lab tests

Researchers Discover Gut Molecule That Powerfully Fights Diabetes

 

You are already at risk for Parkinsons due to your stroke so make sure your doctor prevents diabetes.

Parkinson’s Disease May Have Link to Stroke March 2017 

Convincing evidence that type 2 diabetes is associated with increased risk of Parkinson's

The latest here:

Researchers Discover Gut Molecule That Powerfully Fights Diabetes

Role of human urinary kallikrein in reducing progressive ischemic stroke among acute ischemic stroke patients with concurrent hypertension and diabetes: a hospital-based retrospective cohort study

Where is the protocol located so all stroke hospitals will find and implement it? Oh, you INCOMPENTLY DIDN'T DO THAT? You're fired!

 Role of human urinary kallikrein in reducing progressive ischemic stroke among acute ischemic stroke patients with concurrent hypertension and diabetes: a hospital-based retrospective cohort study

Zeyang Zheng^†Yuelong Li^†Shanshan YangYuanqi XuLian YiYushuang LiuLi ZhangZhongling Zhang^*

• Department of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China

Background: Progressive ischemic stroke (PIS) poses significant challenges in the management of acute ischemic stroke (AIS), with higher morbidity and mortality rates, especially among patients with vascular risk factors such as hypertension and diabetes. This study evaluates the efficacy of human urinary kallidinogenase (HUK) in reducing the incidence of PIS in patients with AIS, with a particular focus on subgroups based on vascular pathology and thrombolytic treatment.

Methods: This retrospective cohort study included 916 patients with AIS treated at a single tertiary care center between January 2022 and September 2023. The patients were divided into two groups based on whether they received HUK treatment in addition to standard care or standard care alone. The primary outcome was the incidence of PIS. Independent sample t-tests or chi-squared tests were used for univariate analysis between groups to identify potential predictors associated with the occurrence of PIS, with factors achieving a p-value < 0.1 considered for multivariate binary logistic regression analysis. Multivariate analysis adjusted for potential confounders to determine independent predictors significantly associated with PIS. The significance threshold was set at p < 0.05. In addition, subgroup analyses were conducted based on stroke subtype (TOAST classification), thrombolysis treatment, and infarction location.

Results: HUK treatment significantly reduced the incidence of PIS (p < 0.001), with the most notable effects observed in patients with large-artery atherosclerosis and small-artery occlusion, those not undergoing intravenous thrombolysis, and those with anterior circulation infarctions. Conversely, no significant reduction was noted in patients with cardioembolic stroke, other etiologies of infarction, intravenous thrombolysis, posterior circulation infarctions, or both anterior and posterior circulation infarctions. Factors such as low body mass index (BMI) and high activated partial thromboplastin time are associated with an increased risk of PIS.

Conclusion: HUK treatment appears to be an effective strategy for reducing the risk of PIS in patients with AIS, particularly in those at higher risk owing to specific vascular pathologies. These findings support the use of HUK in clinical practice to improve the outcomes of patients with stroke. Future prospective, multicenter, randomized controlled trials are warranted to validate these findings and further elucidate the underlying mechanisms.

1 Introduction

Stroke remains the second leading cause of death worldwide and the third most common cause of disability and mortality. Ischemic strokes, representing 62.4% of all new stroke cases, disproportionately affect populations in low to upper-middle-income countries, accounting for over 80% of stroke-related disability-adjusted life years (DALYs) (1). Notably, approximately 25 to 33% of stroke survivors develop PIS within days following the initial event, presenting with worsening neurological deficits and generally poorer prognostic outcomes (2).

HUK, a serine protease derived from urine, has garnered attention for its therapeutic potential in AIS, primarily through enhancing collateral circulation, stimulating angiogenesis, and improving cerebral perfusion (3–5). A longitudinal study involving 300 patients demonstrated that those receiving HUK exhibited notably lower scores on the modified Rankin Scale (mRS) at a 12-month follow-up compared to their counterparts in the control group (6). Moreover, a meta-analysis incorporating data from 24 studies quantified the neurologic improvement attributable to HUK, indicating a 0.56-fold increase in recovery rates (7). Focusing on patients with large artery atherosclerosis, another retrospective analysis revealed that HUK treatment was associated with significantly reduced National Institutes of Health Stroke Scale (NIHSS) scores (8).

Hypertension and diabetes are prevalent risk factors in the AIS patient demographic, with the National Inpatient Sample highlighting that 79% of these patients suffer from hypertension, and 34% are diabetic (9–11). Endothelial dysfunction, insulin resistance, and impaired vascular reactivity caused by hypertension and diabetes may increase the adverse risks in AIS patients. Previous studies have demonstrated that blood pressure levels in AIS patients are significantly associated with their neurological outcomes. Maintaining appropriate blood pressure levels can significantly improve the prognosis of AIS patients (12, 13). Given the high prevalence of these comorbidities and their significant impact on stroke outcomes, investigating the therapeutic potential in this high-risk subgroup is of great clinical significance. Despite these statistics, research into HUK’s effectiveness specifically for patients with AIS concurrently diagnosed with these conditions remains sparse. One study reported that patients with AIS with stage 3 hypertension undergoing HUK treatment showed substantial improvements in mRS scores and recovery rates 3 months post-treatment (14). Another study contrasting patients with AIS with abnormal glucose metabolism observed a significant reduction in NIHSS scores following HUK treatment, although mRS scores did not differ significantly between the treated and control groups (15).

Thus, the present study aimed to investigate the effects of HUK on the incidence of PIS post-admission in patients with AIS with both hypertension and with diabetes, with a subgroup analysis by site of lesions, TOAST subtypes, and the use of intravenous thrombolysis.

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