This Daily Health Metric May Be the Biggest Driver of Brain Aging

 Ask your competent? doctor PRECISELY which glucose monitor to get and what to track. This is all just guidelines(NOT PROTOCOLS!) which tell you nothing actionable.

This Daily Health Metric May Be the Biggest Driver of Brain Aging

If you've been thinking about your brain health, you might already be tracking sleep, stress, or your omega-3 intake. But a large new study suggests there's another number worth paying attention to, one most people only associate with diabetes risk.

Blood glucose. And according to researchers, it may be the single most important metabolic marker when it comes to how fast your brain ages.

About the study

We've known blood sugar affects the body, but its specific relationship to brain aging, across a general population, is still being mapped. This study set out to do exactly that.

Here's how it worked:

• Brain age predictions: Researchers used machine learning to analyze brain MRI scans from healthy participants, training a model to estimate how old a brain looks based on its structure.

• Brain age gap: They applied those predictions across 37,458 people to calculate each person's "brain age gap" (how much older or younger your brain appears compared to your actual age). A positive gap means your brain is aging faster than expected.

• Blood marker analysis: From there, they looked at blood data from more than 21,000 people to find which markers were most closely tied to that gap.

All data came from the UK Biobank, one of the largest health research databases in the world.

Glucose came out on top

Out of nine blood markers that showed a meaningful connection to brain aging, glucose stood out the most.

To make sure this wasn't just a coincidence, researchers used a technique called Mendelian randomization, basically a way of using people's genetic data to test whether one thing is actually causing another, rather than just happening to appear alongside it.

The result?

There's real evidence that elevated glucose may be actively driving faster brain aging, not just tagging along for the ride.

Higher glucose levels were also linked to shrinkage across 80 different brain regions, areas tied to memory, movement, and mood. And people with higher glucose tended to score lower on tests of thinking ability, physical function, and mental health.

The brain conditions connected to glucose

The findings didn't stop at brain aging in general. Higher blood glucose was linked to seven specific brain-related conditions:

• All-cause dementia: an umbrella term for all types of dementia

• Alzheimer's disease: the most common form of dementia

• Vascular dementia: dementia caused by reduced blood flow to the brain

• Parkinson's disease: a progressive condition that affects movement and coordination

• Stroke: when blood supply to part of the brain is cut off

• Depression: a mood disorder with well-established connections to brain structure

• Anxiety: closely tied to changes in brain function over time

That's a wide-ranging list, spanning memory disorders, movement conditions, and mental health, which suggests blood sugar's impact on the brain goes far beyond any one condition.

This isn't just a diabetes story

You don't need a diabetes diagnosis for blood sugar to matter to your brain.

Think of it less like an on/off switch and more like a dial. The lower you can keep that dial, the more you may be protecting your brain for the long haul.

How to keep your glucose working in your brain's favor

Blood sugar balance is one of the most modifiable numbers in your health profile, and the habits that support it aren't complicated. A few evidence-informed places to start:

• Prioritize protein at every meal: Protein slows digestion and softens the blood sugar spike that follows eating; aim to include a quality source (eggs, fish, legumes, poultry) at every meal.

• Add fiber to your plate: Fiber from vegetables, legumes, and whole grains slows how quickly glucose enters your bloodstream, helping keep levels steadier throughout the day; for foods that support blood sugar balance, there are some well-researched options worth knowing.

• Move after meals: Even a 10-minute walk after eating can reduce the blood sugar spike that follows a meal; it doesn't have to be a workout, just movement.

• Pair your carbs: Eating refined carbohydrates on their own sends glucose levels surging; pairing carbs with fat, fiber, or protein softens that response.

• Consider tracking your glucose: Continuous glucose monitors (CGMs) are small wearable sensors that track your blood sugar in real time and can show you exactly how your body responds to specific foods, sleep, and stress.

The takeaway

Of all the metabolic markers researchers tested, glucose had the strongest link to how fast the brain ages, and the connection extended to seven brain-related conditions, from dementia to depression.

That makes blood sugar one of the most compelling levers for brain health, and one of the most actionable.

Scientists Uncover How Glucose Influences Myelin Formation and Function

 Your competent? doctor has informed you of the EXACT DAMAGE to your myelin post stroke and the EXACT PROTOCOLS TO FIX THAT, right? Oh NO, nothing of the sort? So your doctor is ignoring your damage and doing nothing? Sounds like vast incompetence to me!

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Scientists Uncover How Glucose Influences Myelin Formation and Function

Glucose Levels Signal the Growth of Myelin

 

Ask your competent? doctor EXACTLY how much myelin damage you have post stroke and THE EXACT PROTOCOLS TO FIX THAT DAMAGE!

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Glucose Levels Signal the Growth of Myelin

Summary: Scientists have long wondered why myelin, the brain’s essential insulation, develops at different speeds in different regions. A new study reveals that glucose isn’t just fuel; it’s a traffic signal.

High sugar levels tell stem-like cells to multiply, while low sugar levels signal them to stop dividing and start maturing into myelin-forming cells. This metabolic “gear shift” ensures the brain’s wiring is built at exactly the right time and place.

Key Facts

• The Glucose Signal: In the developing brain, regions with high glucose levels act as nurseries for Oligodendrocyte Progenitor Cells (OPCs), causing them to divide rapidly. When glucose levels drop, these cells receive the signal to mature into myelin-producing oligodendrocytes.
• The ACLY Enzyme: The researchers identified an enzyme called ATP-citrate lyase (ACLY) as the key translator. It turns glucose into a molecule (acetyl-CoA) that enters the cell nucleus to “turn on” the genes needed for multiplication.
• Metabolic Switch: Once the cells mature, they stop relying on glucose for development. Instead, they switch to alternative fuels like ketone bodies to actually build the myelin membrane.
• Ketogenic Rescue: In mice lacking the ACLY enzyme, myelin production was stunted. However, when these mice were placed on a ketogenic diet, the alternative fuel source bypassed the glucose bottleneck and improved the myelin deficits.
• Critical Windows: The developmental stage studied (32–40 weeks in human gestation) is a high-risk period for premature babies. Understanding this metabolic signal could lead to new ways to protect the white matter of preemies.

Source: CUNY

Researchers at the Advanced Science Research Center at the CUNY Graduate Center (CUNY ASRC) have uncovered a surprising link between low brain sugar levels and the development of myelin — the protective coating that allows nerve cells to communicate rapidly and efficiently.

The study, set for publication in Nature Neuroscience, reveals that the glucose-sensing ability of stem-like cells during early development helps them determine whether they should multiply and remain undifferentiated or mature into myelin-forming cells, thereby shaping brain development.

Myelin is the membrane of specialized cells called oligodendrocytes, which arise from progenitor cells, called oligodendrocyte progenitor cells (OPCs). Myelination begins before birth and continues into adulthood, supporting critical milestones such as sitting, crawling, walking, and talking.

Scientists have long puzzled over why myelin forms at different times in different brain regions. The CUNY ASRC team discovered that local changes in glucose (the brain’s main energy source) act as a signal that directs behavior during development.

Using advanced technology at the CUNY ASRC MALDI Imaging Core Facility (co-directed by professors Rinat Abzalimov and Ye He), the researchers mapped glucose levels across developing mouse brains. They found that glucose levels vary by region and over time. Areas with higher glucose levels had more actively dividing OPCs while areas with lower glucose levels contained cells beginning to mature into myelin-producing oligodendrocytes.

“Our findings show that glucose is not just fuel for the brain, it’s also a signal for the cells to divide,” said lead author Sami Sauma, a postdoctoral researcher with the CUNY ASRC Neuroscience Initiative who received his Ph.D. from Graduate Center.

“We found that when glucose levels are high in a particular brain region, progenitors use it to drive proliferation. As glucose levels shift, the same cells switch gears and begin maturing. It’s a beautifully coordinated metabolic system that helps shape brain development.”

At the center of this process is an enzyme called ATP-citrate lyase (ACLY). ACLY converts glucose-derived molecules into acetyl-CoA in the cell nucleus, enabling chemical changes to DNA-associated proteins that activate genes required for cell proliferation.

When the researchers genetically deleted ACLY in OPCs, those cells could no longer multiply effectively. As a result, mice showed a temporary reduction in myelin due to a smaller pool of progenitor cells. Remarkably, however, the cells were still able to mature into myelin-producing oligodendrocytes by switching to alternative metabolic sources.The team discovered that while progenitor cells depend on glucose-derived acetyl-CoA to multiply, mature oligodendrocytes rely on acetyl-CoA generated outside the nucleus from other fuels, such as ketone bodies, to produce myelin.

In fact, when transgenic mice lacking the ACLY enzyme in OPCs were placed on a ketogenic diet, which increases ketone levels in the blood, their myelin deficits improved.

“This study reveals that the same cell lineage interprets different metabolic signals at distinct stages of development,” said Patrizia Casaccia, founding director of the CUNY ASRC Neuroscience Initiative and Einstein Professor of Biology at the CUNY Graduate Center.

“By understanding how glucose and alternative energy sources regulate proliferation and myelin formation, we are uncovering new metabolic strategies that could be harnessed to protect myelin in the developing brain and even promote repair in disease states.”

The developmental window studied in mouse models corresponds to approximately 32 to 40 weeks of human gestation, which is a critical period when premature birth can result in white matter injury. The findings suggest that metabolic support during this vulnerable stage could help protect progenitor cells responsible for building myelin.

The implications may also extend to neurological disorders characterized by myelin loss in children and adults, including multiple sclerosis. By targeting the metabolic pathways that regulate progenitor cell proliferation and oligodendrocyte maturation, researchers may be able to design new therapies to enhance myelin repair.

As scientists continue to uncover how metabolism shapes brain development, this research highlights a powerful and potentially modifiable influence on how the brain builds its essential wiring.

Funding: The study was supported by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health.

Key Questions Answered:

Q: Does “low brain sugar” mean I should avoid sugar during pregnancy?

A: No. “Low sugar” in this context refers to localized, natural metabolic shifts within specific brain regions as they develop. This study is about how cells sense sugar, not a recommendation to change dietary intake. The brain always requires a steady supply of glucose to function.

Q: Could a ketogenic diet help treat myelin-related diseases like MS?

A: The study found that ketones can provide an alternative “fuel” for myelin formation when the primary glucose pathway is broken. While this is promising for neonatal brain injury and potentially Multiple Sclerosis, more research is needed before the ketogenic diet can be prescribed as a standardized clinical treatment for myelin repair.

Q: Why do different parts of the brain develop myelin at different times?

A: This study provides a major clue: glucose levels vary across the brain in a timed sequence. By mapping these “glucose gradients,” researchers showed that the brain essentially uses sugar levels to orchestrate the construction of its electrical wiring in a specific, prioritized order.

Editorial Notes:

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

Author: Shawn Rhea
Source: CUNY
Contact: Shawn Rhea – CUNY
Image: The image is credited to Sami Sauma

Original Research: Closed access.
“Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation” by Sami Sauma, Stephanie Stransky, Ipek Selcen, Simone Sidoli, Rinat Abzalimov, Ye He & Patrizia Casaccia. Nature Neuroscience
DOI:10.1038/s41593-026-02263-7

Performance of Continuous Glucose Monitoring System Among Patients With Acute Ischaemic Stroke Treated With Mechanical Thrombectomy

 Your competent? doctor has determined a long time ago how to ensure proper glucose levels post stroke. Oh, you don't have a competent doctor, do you?

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? I'm curious why you haven't solved the glucose problem post stroke.

Healthy Glucose Levels Key to a Healthy Aging Brain September 2017

The latest here:

Performance of Continuous Glucose Monitoring System Among Patients With Acute Ischaemic Stroke Treated With Mechanical Thrombectomy

• November 2024
• Diabetes/Metabolism Research and Reviews 40(8):e70001

DOI:10.1002/dmrr.70001

Authors:

Jie Shi

Jiahao Weng

Yu Ding

• University of Science and Technology of China

Yue Xia

Show all 14 authors

To read the full-text of this research, you can request a copy directly from the authors.

Abstract

Aims 

Glucose metabolism abnormalities are prevalent in acute ischaemic stroke (AIS) patients and are associated with poor prognosis. The continuous glucose monitoring (CGM) system can provide detailed information on glucose levels and glycaemic excursions. This study aimed to evaluate the feasibility and accuracy of CGM application in the acute phase of AIS patients. 

Methods 

This single‐centre, prospective, and observational study consecutively enrolled patients with AIS with anterior circulation large vessel occlusion (AC‐LVO) and received mechanical thrombectomy (MT) within 24 h of symptom onset. A user‐retrospectively calibrated iPro2 CGM system was implanted right before the MT procedure started and removed on the fifth day after MT or at discharge. Fingertip glucose was measured as a reference. Accuracy evaluation included the Bland–Altman plot (with a proportion of CGM values within 15/15, 20/20 and 30/30), the absolute relative difference (ARD) and error grid analysis (EGA). The safety and glucose profiles were also evaluated. 

Results 

Of the 183 patients screened, 141 were included, with a median monitoring duration of 4.49 days. Compared to reference measurements, 3097 CGM readings were matched with a mean bias of −4.16 mg/dL. The proportions of sensor readings meeting the 15/15, 20/20 and 30/30 criteria were 64.55%, 76.07% and 87.21%, respectively. The overall mean and median ARD were 14.60% ± 14.62% and 9.77% (4.15, 20.00). EGA showed that 98.97%, 99.42% and 99.06% values fall within clinically accurate zones in Clarke, Parkes and continuous glucose EGA, respectively. 

Conclusion 

The CGM system was feasible, safe and accurate for in‐hospital use among AIS patients who received MT.

Role of glucose metabolism in Alzheimer’s disease

 Between this earlier research and this, what does your competent? doctor say you should be doing? Not knowing and not answering this is grounds for firing them.

In Neurodegenerative Diseases, Brain Immune Cells Have a Ravenous Appetite for Sugar  October 2021

The latest here:

Role of glucose metabolism in Alzheimer’s disease

At a Glance

• Researchers found that proteins involved in Alzheimer’s disease inhibit glucose metabolism in the brain.
• Blocking a particular enzyme restored glucose metabolism and cognitive function in mouse models of Alzheimer’s disease.
• The findings suggest a novel potential approach for Alzheimer’s disease treatment.

Astrocytes (center) play a crucial role in supporting neurons (top). ART-ur / Shutterstock

In Alzheimer’s disease (AD), misfolded amyloid β (Aβ) and tau proteins accumulate in the brain. This leads to the progressive loss of connections between neurons. At the same time, glucose metabolism declines in certain types of brain cells, called astrocytes and microglia. One function of astrocytes is to help ensure that neurons have enough energy to support their activity. Astrocytes do this by breaking down glucose into lactate and exporting it to neurons. Neurons can then use the lactate as fuel.

Recent research has implicated an enzyme in astrocytes, called indoleamine-2,3-dioxygenase 1 (IDO1), in AD. A team of researchers, led by Dr. Katrin Andreasson at Stanford University, examined how IDO1 affects glucose metabolism in astrocytes. They also looked at how IDO1 and glucose metabolism relate to AD pathology and brain function. The study, which was funded in part by NIH, appeared in Science on August 23, 2024.

The team found that Aβ and tau increased IDO1 levels and activity in astrocytes from both mice and humans. The proteins also suppressed the conversion of glucose to lactate. Inhibiting IDO1 with a drug, or turning off the gene that encodes IDO1, restored lactate production in the presence of Aβ and tau.

The hippocampus is the brain region responsible for learning and memory. In various mouse models of AD, the team found that lactate production in the hippocampus was suppressed. The mice also had impaired spatial memory and low hippocampal synaptic plasticity (the ability of connections between neurons to strengthen over time). Inhibiting IDO1 restored all three of these to normal levels. But inhibiting IDO1 had no effect on synaptic plasticity when neurons were blocked from importing lactate. This suggests that lactate in the hippocampus is important for spatial memory and plasticity.

To see if these findings also applied to AD in humans, the team derived stem cells from people with and without late-onset AD. They then induced the stem cells to form astrocytes and neurons. Glucose metabolism and lactate production were reduced in the astrocytes derived from AD patients. The astrocytes also didn’t effectively transfer lactate to neurons. Inhibiting IDO1 restored lactate production in the astrocytes and its uptake by neurons to normal levels.

The findings suggest that Aβ and tau boost IDO1 activity in astrocytes. This reduces glucose metabolism and lactate production. The loss of lactate, in turn, deprives neurons of an important fuel source.

Restoring lactate production by inhibiting IDO1 might prevent or even reverse the cognitive effects of AD. IDO1 inhibitors have already been developed for cancer treatment and might be repurposed for AD treatment.

“We also can’t overlook the fact that we saw this improvement in brain plasticity in mice with both amyloid and tau mice models,” Andreasson notes. “These are completely different pathologies, and the drugs appear to work for both. That was really exciting to us.”

That suggests that different pathologies may damage neurons via a common mechanism. Thus, this treatment approach could potentially work not only for AD, but for other neurodegenerative diseases as well.

—by Brian Doctrow, Ph.D.

Brain rejuvenation breakthrough: How limiting glucose could spark new neuron growth

 But isn't your doctor already using one of these on you?

Young Blood Revitalizes the Aging Brain June 2014 

Characterizing the Mechanism of Young Bone Marrow Derived Microglia-Like Cells on Restoring Cognitive Function in the Aged Brain and After Ischemic Injury

March 2022 

Or this:

Young brain fluid improves memory in old mice October 2022

The latest here:

Brain rejuvenation breakthrough: How limiting glucose could spark new neuron growth

STANFORD, Calif. — Could the secret to maintaining a youthful, sharp mind be as simple as watching our sugar intake? A new study from Stanford Medicine suggests that glucose plays a surprising role in the aging brain’s ability to produce new neurons.

As we age, our brains become less adept at producing new neurons, a process known as neurogenesis. This decline can have far-reaching consequences, contributing to memory loss, reduced cognitive function, and potentially exacerbating neurodegenerative diseases like Alzheimer’s and Parkinson’s. It also hinders recovery from stroke and other brain injuries. However, this new research, led by Anne Brunet, PhD, professor of genetics, offers hope by shedding light on why neural stem cells – the precursors to new neurons – become less active with age.

Using cutting-edge CRISPR technology, Brunet and her team conducted a comprehensive genetic screen to identify genes that, when inhibited, could reactivate dormant neural stem cells in aged mice. Among the 300 genes they discovered, one stood out: Slc2a4, which codes for the glucose transporter protein GLUT4.

“We first found 300 genes that had this ability— which is a lot,” Brunet explains in a statement. “One in particular caught our attention. It was the gene for the glucose transporter known as the GLUT4 protein, suggesting that elevated glucose levels in and around old neural stem cells could be keeping those cells inactive.”

To validate their findings in living animals, the researchers developed an innovative in vivo screening technique. They injected viruses carrying genetic instructions to knock out specific genes into the subventricular zone of aged mouse brains – an area rich in neural stem cells. After five weeks, they examined the olfactory bulb, where newly generated neurons typically migrate.

The results, published in the journal Nature, were dramatic. Knocking out the Slc2a4 gene led to a more than two-fold increase in new neuron production in the olfactory bulbs of old mice. This boost in neurogenesis was accompanied by an increase in both quiescent and activated neural stem cells in the subventricular zone, indicating that the treatment was stimulating the stem cell population itself.

Among the 300 genes researchers discovered, one stood out: Slc2a4, which codes for the glucose transporter protein GLUT4. (© vegefox.com – stock.adobe.com)

Further investigation revealed that neural stem cells from older mice take up about twice as much glucose as those from young mice. This increased glucose uptake appears to push the stem cells into a more dormant state. By knocking out Slc2a4 and reducing glucose influx, the aged stem cells became more likely to activate and produce new neurons.

“It’s allowing us to observe three key functions of the neural stem cells. First, we can tell they are proliferating. Second, we can see that they’re migrating to the olfactory bulb, where they’re supposed to be. And third, we can see they are forming new neurons in that site,” explains Tyson Ruetz, PhD, lead author of the study and former post-doctoral scholar in Brunet’s lab, in a media release.

The glucose transporter connection opens up exciting possibilities for future interventions. Brunet described it as “a hopeful finding,” suggesting that it could lead to the development of pharmaceutical or genetic therapies to stimulate new neuron growth in aged or injured brains. Perhaps even more intriguingly, it raises the possibility of simpler behavioral interventions, such as a low-carbohydrate diet, that might adjust the amount of glucose taken up by old neural stem cells.

While this research marks a significant step forward in our understanding of brain aging and regeneration, it’s important to note that the study was conducted in mice. Further research is needed to determine if these findings translate to humans and to explore the long-term effects and potential side-effects of manipulating glucose uptake in neural stem cells.

Nevertheless, this study provides a promising new direction for addressing age-related cognitive decline and potentially treating neurodegenerative diseases. By identifying GLUT4 and other key regulators of neural stem cell aging, scientists now have promising new targets for developing therapies to rejuvenate the aging brain.

Paper Summary

Methodology

The researchers used CRISPR-Cas9 gene editing technology to systematically knock out over 20,000 genes in cultured neural stem cells from young and old mice. They then assessed which gene knockouts enhanced the stem cells’ ability to activate and divide. To test the most promising gene candidates in living mouse brains, they developed a novel in vivo screening technique. This involved injecting viruses carrying CRISPR components to knock out specific genes in the subventricular zone of aged mouse brains. Five weeks later, they examined the olfactory bulb to quantify newly generated neurons containing the genetic knockouts.

Key Results

The in vitro screen identified over 300 genes that, when inhibited, boosted the activation of aged neural stem cells. The in vivo screen validated 24 of these genes, with Slc2a4 consistently emerging as a top hit. Knocking out Slc2a4 in the brains of old mice increased new neuron production in the olfactory bulb by more than two-fold. It also increased the numbers of both quiescent and activated neural stem cells in the subventricular zone. Further experiments revealed that aged neural stem cells take up about twice as much glucose as young ones and that this elevated glucose uptake appears to promote quiescence.

Study Limitations

The study was conducted in mice, so it remains to be seen if the findings will translate to humans. The researchers focused on the subventricular zone, but it’s unclear if similar mechanisms apply to other neurogenic regions like the hippocampus. The long-term effects and potential side effects of Slc2a4 inhibition were not evaluated. Additionally, while the screening approach was powerful, it may have missed some important genes.

Discussion & Takeaways

This study provides strong evidence that elevated glucose uptake contributes to the decline in neural stem cell function during aging. By identifying GLUT4 as a key regulator of this process, the researchers have uncovered a promising new target for potential therapies to enhance neurogenesis in aged brains. The fact that brief glucose starvation could activate aged stem cells suggests dietary interventions might offer a non-invasive way to boost neurogenesis. However, much more research is needed to determine if modulating glucose uptake in neural stem cells could safely and effectively enhance cognitive function or treat neurodegenerative diseases in humans.

Funding & Disclosures

The study was supported by grants from the National Institutes of Health (grants P01AG036695 and R01AG056290), the Stanford Brain Rejuvenation Project and a Larry L. Hillblom Foundation Postdoctoral Fellowship. Tyson Ruetz, the lead author, is now the scientific advisor and co-founder of ReneuBio.

Blood Sugar May Be Key to Brain Power After a Stroke

Will this prompt your stroke hospital to create protocols for testing this and then followup protocols to prevent cognitive decline from happening? Or is your hospital incompetent in not even knowing about this?

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

 

Blood Sugar May Be Key to Brain Power After a Stroke

By Cara Murez HealthDay Reporter

(HealthDay)

FRIDAY, May 19, 2023 (HealthDay News) -- Having higher blood sugar can lead to quicker loss of brain power after a stroke, a new study suggests.

High blood pressure and cholesterol were not associated with a similar mental loss, even in those at higher genetic risk for dementia.

“Having a stroke increases a person’s risk of dementia up to 50-fold, but we lack a comprehensive treatment approach that could reduce this risk, other than preventing a second stroke,” said study co-author Dr. Deborah Levine, a professor of medicine and neurology at the University of Michigan Medical School.

“These findings suggest that higher cumulative blood sugar levels after stroke contribute to faster cognitive decline, and hyperglycemia [excess blood sugar] after stroke, regardless of diabetes status, could be a potential treatment target to protect post-stroke cognition,” Levine said in a Michigan Health news release.

Researchers used data from the STROKE COG study, which pooled data from four long-term U.S. studies. The new study looked at nearly 1,000 people whose measurements of brain function and blood tests were taken for years before and after they had a stroke.

Stroke survivors with high blood sugar had a much quicker loss of general thinking ability. However, high blood sugar did not affect executive function (complex decision-making ability) or memory, according to the study.

The team adjusted the data for differences in factors such as age, income, education, and use of medications to treat high blood pressure, cholesterol and blood sugar. Post-stroke blood sugar measurements were taken an average of two years after their first stroke. About 20% of the study participants were taking diabetes medication before their stroke.

Further research is needed to test whether tight blood sugar control in stroke survivors reduces this post-stroke cognitive decline and dementia, in people with and in those without diagnosed diabetes, Levine said.

Tight blood sugar control in people with diabetes is known to reduce small blood vessel complications in the eyes, kidneys and nerves. It might also reduce small blood vessel disease in the brain, the researchers suggested, though this is unproven.

People who have survived strokes and mini-strokes should work with their health care team to determine the best approach to testing and managing blood sugar for them, according to the researchers. This is especially true if they have pre-diabetes or diabetes.

Very low blood sugar levels in older adults are also a risk for dementia and should be avoided, Levine said.

The study was funded by the U.S. National Institute in Aging and other sources. The results were published online May 17 in JAMA Network Open.

More information

The American Stroke Association has more on life after a stroke.

SOURCE: Michigan Medicine, news release, May 17, 2023

Higher Glucose Levels May Contribute to Faster Cognitive Decline in Stroke Survivors

Will this prompt your stroke hospital to create protocols for testing this and then followup protocols to prevent cognitive decline from happening? Or is your hospital incompetent in not even knowing about this?

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

Higher Glucose Levels May Contribute to Faster Cognitive Decline in Stroke Survivors

Higher cumulative glucose levels may contribute to faster cognitive decline in stroke survivors, representing a potential treatment target to preserve cognition after stroke, according to a study published in JAMA Network Open.

“Having a stroke increases a person’s risk of dementia up to 50-fold,

but we lack a comprehensive treatment approach that could reduce this risk, other than preventing a second stroke,” said Deborah A. Levine, MD, University of Michigan Medical School, Ann Arbor, Michigan. “These findings suggest that higher cumulative blood sugar levels after stroke contribute to faster cognitive decline, and hyperglycaemia after stroke, regardless of diabetes status, could be a potential treatment target to protect post-stroke cognition.”

Dr. Levine and colleagues evaluated associations of post-stroke systolic blood pressure (BP), glucose, and low-density lipoprotein (LDL) cholesterol levels with cognitive decline by conducting a meta-analysis of 4 US cohort studies (conducted 1971-2019) that included 982 dementia-free individuals (48.9% female; 29.4% Black).

The median age at incident stroke was 74.6 years. Cumulative mean post-stroke systolic BP and LDL cholesterol levels were not associated with any cognitive outcome. However, after accounting for cumulative mean post-stroke systolic BP and LDL cholesterol levels, higher cumulative mean post-stroke glucose level was associated with faster decline in global cognition (-0.04 points/y faster per each 10 mg/dL increase; P = .046) but not executive function or memory.

After restricting to 798 participants with apolipoprotein E4 (APOE4) data and controlling for APOE4 and APOE4 × time, higher cumulative mean post-stroke glucose level was associated with a faster decline in global cognition in models without and with adjustment for cumulative mean post-stroke systolic BP and LDL cholesterol levels (-0.05 points/y faster per 10 mg/dL increase, P = .01; -0.07 points/y faster per 10 mg/dL increase, P = .002) but not executive function or memory declines.

Dr. Levine noted that the new study suggests the need for clinical research to test whether tight glycaemic control in stroke survivors reduces post-stroke cognitive decline and dementia in those with and without diagnosed diabetes.

Tight glycaemic control has been shown in people with diabetes to reduce small blood vessel complications in the eyes, kidney, and nerves, and may have the potential to also decrease small blood vessel disease in the brain, but this is unproven.

Reference: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2805003

SOURCE: Michigan Medicine - University of Michigan

In Neurodegenerative Diseases, Brain Immune Cells Have a Ravenous Appetite for Sugar

 So what is the takeaway from this news?  Should we be going directly to a keto diet at the first sign of MCI?

Don't listen to me, I'm not medically trained. Demand your doctor  definitively answer this question, no heming or hawing.

Your doctor should have been working on micro-glia for two years already

Inflammation within the Neurovascular Unit: Focus on Microglia for Stroke Injury and Recovery July 2019

Or are you allowing nothing to be done to solve stroke by your doctors?

In Neurodegenerative Diseases, Brain Immune Cells Have a Ravenous Appetite for Sugar

Summary: In the early stages of neurodegenerative diseases, microglia consume glucose to a greater extent than previously believed. The findings may serve as a new biomarker for a range of neurodegenerative disorders.

Source: DZNE

At the beginning of neurodegenerative disease, the immune cells of the brain – the “microglia” – take up glucose, a sugar molecule, to a much greater extent than hitherto assumed.

Studies by the DZNE, the LMU München and the LMU Klinikum München, published in the journal Science Translational Medicine, come to this conclusion.

These results are of great significance for the interpretation of brain scans depicting the distribution of glucose in the brain. Furthermore, such image-based data could potentially serve as a biomarker to non-invasively capture the response of microglia to therapeutic interventions in people with dementia.

In humans, the brain is one of the organs with the highest energy consumption, which can change with age and also due to disease – e. g. as a result of Alzheimer’s disease.

“Energy metabolism can be recorded indirectly via the distribution of glucose in the brain. Glucose is an energy carrier. It is therefore assumed that where glucose accumulates in the brain, energy demand and consequently brain activity is particularly high,” says Dr. Matthias Brendel, deputy director of the Department of Nuclear Medicine at LMU Klinikum München.

The measuring technique commonly used for this purpose is a special variant of positron emission tomography (PET), known as “FDG-PET” in technical jargon. Examined individuals are administered an aqueous solution containing radioactive glucose that distributes in the brain. Radiation emitted by the sugar molecules is then measured by a scanner and visualized.

“However, the spatial resolution is insufficient to determine in which cells the glucose accumulates. Ultimately, you get a mixed signal that stems not only from neurons, but also from microglia and other cell types found in the brain,” says Brendel.

Cellular Precision

“The textbook view is that the signal from FDG-PET comes mainly from neurons, because they are considered the largest consumers of energy in the brain,” says Christian Haass, research group leader at DZNE and professor of biochemistry at LMU Munich.

“We wanted to put this concept to the test and found that the signal actually comes predominantly from the microglia. This applies at least in the early stages of neurodegenerative disease, when nerve damage is not yet so advanced. In this case, we see that the microglia take up large amounts of sugar. This appears to be necessary to allow them for an acute, highly energy-consuming immune response. This can be directed, for example, against disease-related protein aggregates. Only in the later course of the disease does the PET signal appear to be dominated by neurons.”

In humans, the brain is one of the organs with the highest energy consumption, which can change with age and also due to disease. Image is in the public domain

The findings of the Munich researchers are based on laboratory investigations as well as PET studies in about 30 patients with dementia – either Alzheimer’s disease or so-called four-repeat tauopathy. The findings are supported, for instance, by studies on mice whose microglia were either largely removed from the brain or, so to speak, deactivated. In addition, a newly developed technique was used that allowed cells derived from the brains of mice to be sorted according to cell type and their sugar uptake to be measured separately.

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