DMT Shows Promise in Protecting the Brain After Stroke

 

 Didn't your competent? doctor start prescribing this years ago? Oh no, incompetence reigned because your doctor doesn't follow stroke research!

Which proves your board of directors is so incompetent they can't recognize crapola in their hospital staff that needs to be removed! YOU need to reconstitute the hospital!

DMT (20  posts to November 2020)

DMT Shows Promise in Protecting the Brain After Stroke

Summary: New research shows that DMT, a natural psychoactive compound found in plants and the human brain, can protect against stroke damage in animal and cell models. Treatment with DMT reduced infarct size, brain swelling, and inflammation, while also repairing blood-brain barrier function.

The compound acted through Sigma-1 receptors to limit microglial activation and support astroglial cells, creating a dual protective effect. These findings suggest DMT could one day serve as an adjuvant therapy for stroke, expanding treatment options and improving recovery outcomes.

Key Facts

• Barrier Protection: DMT restored blood-brain barrier integrity after stroke.
• Inflammation Control: It reduced cytokine production and microglial activation.
• Therapeutic Potential: Could complement limited existing stroke treatments.

Source: HUN-REN BRC

DMT, or dimethyltryptamine is a natural psychoactive molecule found in many plants and mammals.

According to an article published in Science Advances, researchers from the HUN-REN BRC Institute of Biophysics and Semmelweis University Heart and Vascular Centre found that DMT reduces the harmful effects of stroke in animal models and cell culture experiments. 

This psychoactive compound also inhibited the production of inflammatory cytokines in brain endothelial cells and peripheral immune cells, while reduced the activation of brain microglia cells through Sigma-1 receptors. Credit: Neuroscience News

A solution from nature in the spotlight

DMT is also present in the human brain, and it is currently undergoing clinical trials to aid recovery of brain function after stroke. However, its exact mechanism of action had not been fully understood until now. “It is amazing how we can always turn to Nature to find ingenious solutions for health problems” says co-lead author Mária Deli from the HUN-REN BRC.

The blood-brain barrier as a therapeutic target

 “We found that DMT significantly reduced infarct volume and edema formation in a rat stroke model”, explains co-first author Marcell László.

In both animal experiments and cell culture models, the authors showed that DMT treatment restored the structure and function of the damaged blood-brain barrier and improved the function of astroglial cells.

This psychoactive compound also inhibited the production of inflammatory cytokines in brain endothelial cells and peripheral immune cells, while reduced the activation of brain microglia cells through Sigma-1 receptors.

DMT could serve as therapeutic adjuvant to existing stroke treatments 

“The therapeutic options currently available for stroke are very limited. The dual action of DMT, protecting the blood-brain barrier while reducing brain inflammation, offers a novel, complex approach that could complement existing treatments”, says Judit Vigh, co-first author of the work.

Since current stroke therapies do not always result in full recovery, a DMT-based treatment may represent a promising new alternative, mainly in combination with existing methods.

The recent findings from researchers in Szeged and Budapest, Hungary, support the development of a therapy that goes beyond the limitations of conventional stroke treatment. Clinical trials on the use of DMT and investigation on its long-term effects are currently ongoing.

About this neuroscience research news

Author: Anett Nagy-Demcsák
Source: HUN-REN BRC
Contact: Anett Nagy-Demcsák – HUN-REN BRC
Image: The image is credited to Neuroscience News

Original Research: Open access.
“N,N-dimethyltryptamine mitigates experimental stroke by stabilizing the blood-brain barrier and reducing neuroinflammation” by Maria A. Deli et al. Science Advances

Stroke Survivors’ Brains Rejuvenate to Compensate for Injury

 How will your competent? doctor MAKE SURE THIS OCCURS AND DELIVERS 100% RECOVERY?

Stroke Survivors’ Brains Rejuvenate to Compensate for Injury

Summary: In a massive international study, researchers have discovered a surprising pattern of neuroplasticity in stroke survivors. Using deep learning to analyze brain scans from over 500 survivors across eight countries, researchers found that while a stroke accelerates aging in the damaged hemisphere, the undamaged side of the brain actually begins to look “younger” in its structure.

This regional rejuvenation—particularly in areas responsible for motor planning and attention—appears to be the brain’s way of “retooling” healthy networks to compensate for severe physical impairment.

Key Facts

• Brain-PAD Marker: Researchers used AI to calculate the “Brain-Predicted Age Difference” (brain-PAD). A “younger” brain age in undamaged regions served as a sensitive marker for neural reorganization.
• The Contralesional Shift: Survivors with the most severe movement deficits showed the most “youthful” structural patterns in the hemisphere opposite their injury, especially within the frontoparietal network.
• Global Collaboration: The study was part of the ENIGMA Stroke Recovery Working Group, harmonizing data from 34 research sites to create the world’s largest dataset of its kind.
• Paradoxical Adaptation: This youthful shift doesn’t necessarily mean the movement has fully recovered; rather, it reflects the brain physically adapting and “rejuvenating” healthy tissue to pick up the slack for the damaged motor system.

Source: USC

In a new study published in The Lancet Digital Health, scientists at the USC Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) have discovered that the brains of people who experience severe physical impairment after a stroke may reorganize themselves in unexpected ways, showing signs of “younger” brain structure in undamaged regions as they adapt to injury.

The international research effort is part of the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Stroke Recovery Working Group, which analyzed brain scans from more than 500 stroke survivors across 34 research sites in eight countries.

AI analysis reveals that larger strokes accelerate aging in the damaged hemisphere but paradoxically make the opposite side appear younger as it compensates for lost function. Credit: Neuroscience News

Using deep learning models trained on tens of thousands of MRI scans, the researchers estimated the “brain age” of different regions in each hemisphere to see how stroke damage affects brain structure and recovery.

“We found that larger strokes accelerate aging in the damaged hemisphere but paradoxically make the opposite side of the brain appear younger,” said Hosung Kim, PhD, associate professor of research neurology at the Keck School of Medicine of USC and co-senior author of the study.

“This pattern suggests the brain may be reorganizing itself, essentially rejuvenating undamaged networks to compensate for lost function.”

The research team used an advanced form of artificial intelligence known as a graph convolutional network to predict the biological age of 18 brain regions from MRI data. The difference between a person’s predicted brain age and their actual chronological age, known as the brain-predicted age difference (brain-PAD), served as a sensitive marker of neural health.

When the team associated these measurements with motor performance scores, they found a striking pattern: stroke survivors with severe movement deficits, even after more than 6 months of rehabilitation, showed younger-than-expected brain age in regions opposite the lesion, particularly within the frontoparietal network, a key system involved in motor planning, attention, and coordination.

“These findings suggest that when stroke damage leads to greater movement loss, undamaged regions on the opposite side of the brain may adapt to help compensate,” Kim explained.

“We saw this in the contralesional frontoparietal network, which showed a more ‘youthful’ pattern and is known to support motor planning, attention, and coordination. Rather than indicating full recovery of movement, this pattern may reflect the brain’s attempt to adjust when the damaged motor system can no longer function normally. This gives us a new way to see neuroplasticity that traditional imaging could not capture.”

The study was conducted through ENIGMA, a global alliance that unites data from more than 50 countries to better understand the brain across diseases. Researchers harmonized MRI data and clinical measures across dozens of cohorts to build the world’s largest stroke neuroimaging dataset of its kind.

“By pooling data from hundreds of stroke survivors worldwide and applying cutting-edge AI, we can detect subtle patterns of brain reorganization that would be invisible in smaller studies. These findings of regionally differential brain aging in chronic stroke could eventually guide personalized rehabilitation strategies,” said Arthur W. Toga, PhD, director of the Stevens INI and Provost Professor at USC.

The team plans to expand their work to include longitudinal studies tracking patients from the acute to chronic stages of stroke recovery. By observing how patterns of brain aging and reorganization develop over time, clinicians might be able to customize interventions based on each patient’s unique neural adaptation process, ultimately improving recovery outcomes and quality of life in the near future.

Key Questions Answered:

Q: How can a brain actually look “younger” after an injury?

A: It’s not about reversing time, but about structural density and connectivity. The AI models found that in response to a major “clog” or “break” in the motor system, the healthy side of the brain recruits more resources and builds more robust connections, mimicking the flexible, dense structure typically seen in younger brains.

Q: Does a “younger” brain mean a faster recovery?

A: Paradoxically, the “youngest” patterns were seen in those with the most severe physical impairments. This suggests that the brain only hits the “emergency rejuvenation” button when the damage is so extensive that the original motor pathways can no longer function at all.

Q: How will this change how stroke patients are treated?

A: Currently, rehab is often “one size fits all.” By using AI to see which parts of a patient’s brain are trying to “rejuvenate,” doctors could eventually create personalized physical therapy that targets and strengthens those specific healthy networks.

Editorial Notes:

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

About this neurology and stroke research news

Author: Laura LeBlanc
Source: USC
Contact: Laura LeBlanc – USC
Image: The image is credited to Neuroscience News

Migraines May Leave the Brain Vulnerable to Stroke

 Your competent? doctor knew of this risk years ago and DELIVERED EXACT PROTOCOLS TO FIX THE PROBLEM, RIGHT? Sorry, nothing occurred! Well when you have a board of directors so fucking incompetent they can't see what incompetence looks like in staff, then you get nothing!

• migraine (47 posts to February 2011)
• Migraine with aura (13 posts to March 2016)

Migraines May Leave the Brain Vulnerable to Stroke

Summary:

The American Heart Association and the American Headache Society have joined forces to fund high-risk, high-reward research investigating how migraines and headache disorders drive cardiovascular and cerebrovascular decline. The projects aim to discover how recurring migraine attacks prime immune cells, damage cerebral blood vessels, impair brain waste clearance, and escalate stroke risk.

Key Facts:

• Historic Research Partnership: For the first time, the American Headache Society and the American Heart Association are co-funding an Innovative Project Award ($200,000 over two years) alongside three additional AHA-backed grants targeting the intersection of headaches and vascular health.
• Perivascular Macrophages as Stroke Drivers: The flagship co-funded project investigates whether frequent migraines over-activate the brain’s perivascular macrophages—vessel-guarding immune cells—causing vascular weakness that elevates stroke susceptibility.
• Multifaceted Pathological Targets: Additional funded projects will examine cortical spreading depression’s impact on cerebral endothelium, develop contrast-free MRI techniques for idiopathic intracranial hypertension (IIH), and study the choroid plexus in obesity-related migraines.

Source: American Heart Association / American Headache Society

Migraine is far more than a severe headache; it is a complex neurological disorder with well-documented, yet poorly understood, ties to systemic cardiovascular and cerebrovascular disease. Individuals who suffer from chronic migraine, particularly migraine with aura, face an elevated risk of stroke and myocardial infarction.

To unravel the mechanisms underlying this link, the American Headache Society (AHS) and the American Heart Association (AHA) have launched an inaugural joint funding partnership. Together with three standalone awards funded by the AHA, the initiative provides $200,000 over two years for high-risk, high-reward projects across basic science, clinical trials, and population health.

Do Overactive Immune “Guards” Weaken Brain Vessels?

The flagship co-funded award was granted to Juliana Navia Pelaez, Ph.D., an assistant professor at St. Louis University School of Medicine. Her project, “Neurogenic Priming of Perivascular Macrophages by Migraine-Associated Peptides Increases Stroke Risk,” focuses on the brain’s resident immune sentinels.

During a migraine episode, cerebral blood vessels undergo cycles of constriction, dilation, and altered flow. Dr. Pelaez’s laboratory is investigating whether perivascular macrophages—specialized immune cells that envelope and defend cerebral blood vessels—become pathologically hyperactive from repeated attacks.

“If migraines happen over and over, these immune cells might stay ‘on’ for too long. When this happens, they might accidentally make the blood vessels weaker,” said Dr. Pelaez. “If the vessels get weaker, the brain might have a harder time protecting itself from a stroke.”

By tracking how migraine-related neuropeptides trigger these macrophages, the study aims to identify therapeutic targets to calm overactivated immune cells or intercept inflammatory signaling cascades before vascular damage occurs.

Three Additional Projects Advancing Cerebrovascular Discoveries

Alongside Dr. Pelaez’s project, the AHA has funded three additional grants examining critical vascular interfaces in headache disorders:

• Cortical Spreading Depolarization and Endothelial Remodeling:Led by Andrea M. Harriott, M.D., Ph.D., at Massachusetts General Hospital, this project investigates how the neural waves underlying migraine aura (cortical spreading depolarizations) affect cerebral blood vessel linings. The team is analyzing protein shifts, collateral vessel remodeling, and angiogenesis to establish whether long-term aura exposure directly damages the brain’s vascular architecture.
• Glymphatic Clearance in Idiopathic Intracranial Hypertension (IIH):Headed by Matthew T. Bender, M.D., at the University of Rochester, this project addresses IIH, a debilitating disorder marked by elevated intracranial pressure that predominantly affects overweight women of childbearing age. Using a novel, non-invasive, contrast-free quantitative MRI technique, the team will visualize the glymphatic-hemodynamic axis before and after venous sinus stenting to uncover how opening cerebral veins restores waste removal and blood flow.
• The Choroid Plexus in Obesity-Driven Migraine: Led by Neil Dani, Ph.D., at Vanderbilt University, this initiative examines the choroid plexus, the cellular gateway that produces cerebrospinal fluid (CSF), in the rising prevalence of obesity-linked migraines. The study explores whether systemic metabolic inflammation enters the central nervous system via CSF pathways and will test whether clinically approved drugs, such as acetazolamide, can curb neuroinflammation and pain signaling.

By moving beyond symptom suppression to target shared inflammatory, hemodynamic, and glymphatic pathways, these collaborative efforts aim to pioneer preventive interventions that safeguard both brain and cardiovascular health.

Editorial Notes:

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

About this Neurology Research:

• Media Contact: Cathy Lewis
• Source: AHA
• Image Credit: Image credited to Neuroscience News

Insomnia Linked to Significantly Higher Risk of Stroke

 Does your competent? doctor have an EXACT sleep protocol so you don't get insomnia?

Insomnia Linked to Significantly Higher Risk of Stroke

Summary:

An international umbrella review led by the European Academy of Neurology and MedUni Vienna reveals that chronic insomnia is associated with a 26% higher risk of stroke and a 28% increase in hospitalizations. The analysis also identified significant links between persistent sleep disruption and heightened risks for Alzheimer’s disease, depression, and suicidal behavior.

Key Facts:

• Elevated Stroke Risk: A meta-analysis pooling data across more than 1.3 million participants found that individuals suffering from insomnia had a 26% higher risk of experiencing a stroke.
• Increased Hospitalizations: Individuals with insomnia were 28% more likely to be admitted to the hospital compared to those with healthy sleep patterns.
• Brain Health Warning Sign: While direct causality remains unproven, the evidence links insomnia to multiple adverse neuropsychiatric outcomes, including dementia (particularly Alzheimer’s disease), clinical depression, and suicidal behavior.

Source: Medical University of Vienna / European Academy of Neurology

Insomnia is widely recognized for disrupting nightly rest, dulling mental clarity, and impairing day-to-day productivity. However, a comprehensive international investigation led by the European Academy of Neurology (EAN) in collaboration with the Medical University of Vienna (MedUni Vienna) underscores that sleep disturbances may also serve as critical warning indicators for life-threatening vascular, neurological, and mental health conditions.

Published in Sleep Medicine Reviews, the umbrella systematic review evaluated existing epidemiological evidence across seven health endpoints: stroke, dementia, depression, suicidal behavior, mortality, workplace accidents, and hospital admissions. To establish stronger quantitative estimates, the investigators conducted dedicated new meta-analyses specifically targeting stroke, hospitalizations, and occupational accidents.

Concrete Links to Stroke and Hospital Admissions

For the stroke analysis, the research team identified nine studies encompassing more than 1.3 million participants, combining six within an extensive meta-analysis. The results demonstrated that insomnia is associated with a 26% elevated risk of stroke.

A parallel meta-analysis evaluating five studies focused on healthcare utilization discovered that individuals with chronic insomnia were 28% more likely to be hospitalized than individuals without sleep disruption.

Beyond acute cardiovascular and systemic events, the review synthesized multiple systematic reviews connecting insomnia to chronic brain and mental health pathologies. Consistent patterns emerged linking poor sleep to elevated risks of dementia, most notably Alzheimer’s disease, as well as major depression and suicidal behavior, although statistical consistency varied across individual analytical endpoints.

“Sleep should be part of the discussion on brain health at every stage of life. We should raise awareness of insomnia and its treatment and ensure that sleep is also taken into account in health promotion programmes in communities, schools and the workplace,” said study co-author Stefan Seidel, M.D., a neurologist and sleep specialist at MedUni Vienna and medical director of the Pirawarth Clinic, who initiated the study as a member of the EAN.

Interpreting Risk: Correlation, Not Direct Causation

The researchers emphasize that while the observational associations are substantial, the findings do not demonstrate a direct cause-and-effect relationship.

Discrepancies in how insomnia was clinically defined across original studies, combined with confounding variables, such as the underlying use of prescription hypnotics or baseline cardiometabolic status, warrant careful interpretation of individual risk estimates. Nonetheless, the authors conclude that chronic insomnia should no longer be treated as an isolated complaint, but rather prioritized as an early clinical red flag for declining systemic and cognitive health.

Editorial Notes:

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

About this neurology Research:

• Media Contact: Karin Kirschbichler
• Source: Medical University of Vienna
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Sleep Medicine Reviews (Sept 22, 2026). “Insomnia as a risk factor for brain, mental and general health consequences: an umbrella systematic review.” Authors: Luca Vignatelli, Maurizio A. Leone, Elisabetta Pupillo, Stefan Seidel, Ulf Kallweit, Natalia Colorado Prieto, Maria Lolich, Marina Tüzün, and Claudio L. A. Bassetti.
• DOI: 10.1016/j.smrv.2026.102372

Uninjured Brain Age Holds Key to Language Recovery Following Stroke

 Does your doctor have two neurons to rub together to update their aphasia protocols with this? 

They don't have any? PURE INCOMPETENCE!

Uninjured Brain Age Holds Key to Language Recovery Following Stroke

Summary:

A new study demonstrates that accelerated biological aging in areas of the brain spared by a stroke strongly influences language impairment and long-term rehabilitation outcomes. Researchers found that structural brain age in uninjured tissue predicted aphasia severity and forecast language recovery six months after speech therapy paired with brain stimulation.

Key Facts:

• Impact of Non-Injured Tissue: Biological aging patterns in the hemisphere opposite the stroke lesion accounted for aphasia severity independently of the stroke lesion’s actual size or location.
• Predicting Recovery Success: Structural brain aging metrics gathered prior to intervention reliably predicted language improvements six months after patients completed speech therapy paired with noninvasive brain stimulation.
• Accessible Clinical Translation: The predictive framework relies solely on standard, routine brain scans evaluated via a free, open-access online tool trained on normative human aging datasets.

Source: Society for Neuroscience / University of South Carolina Floyd School of Medicine

Following an ischemic or hemorrhagic stroke, neurological damage is rarely restricted strictly to the primary lesion site. Even brain regions that escape direct ischemic injury can exhibit hallmarks of accelerated structural aging. This secondary vulnerability is especially evident in post-stroke aphasia, a debilitating language impairment characterized by vast individual variability in both baseline severity and long-term responsiveness to rehabilitation.

Historically, clinicians have attempted to forecast recovery by mapping the focal stroke injury itself: measuring lesion volume and tracking specific damaged language tracts. However, these metrics often fail to explain why two individuals with nearly identical lesions experience drastically different recovery trajectories.

Now, a study published in The Journal of Neuroscience (JNeurosci) led by Nicholas Riccardi, Leonardo Bonilha, and colleagues from the University of South Carolina Floyd School of Medicine establishes that post-stroke language outcomes depend significantly on the biological age and resilience of uninjured brain tissue.

Machine Learning Reveals the Brain Age Gap

To quantify subtle structural changes across the whole brain, the research team implemented an online machine-learning platform trained on extensive, normative human brain aging datasets. This computational model compares an individual’s structural MRI scan against expected benchmarks to detect biological deviations from chronological aging.

The investigators evaluated 188 post-stroke patients presenting with varying degrees of aphasia. Strikingly, structural aging markers within the hemisphere not directly damaged by the stroke explained aphasia severity independently of classical variables, such as lesion volume or anatomical location.

Furthermore, the team assessed patients undergoing an intensive rehabilitation regimen combining speech-language therapy with noninvasive brain stimulation. Baseline brain aging metrics recorded prior to treatment accurately predicted the extent of sustained language gains measured six months after therapy concluded.

Accessible, Low-Cost Rehabilitation Biomarkers

The findings establish a critical link between baseline biological aging models and post-stroke rehabilitation success, offering an objective framework for tailoring individualized recovery protocols.

Importantly, because the computational model requires only a standard, non-contrast clinical MRI and an accessible, free computational algorithm, the methodology avoids the high technical and financial hurdles that typically stall advanced neuroimaging biomarkers.

“This work suggests that recovery potential after stroke depends on the health of the rest of the brain, which is partly shaped by treatable factors like cardiovascular health,” said lead author Nicholas Riccardi. “Second, because everything here came from a single routine scan and a free online tool, this could realistically reach a variety of clinical or research settings one day.”

Targeting modifiable systemic health factors, such as blood pressure, metabolic markers, and exercise habits, could serve to protect global brain resilience, ensuring that uninjured neural networks remain primed to support post-stroke neuroplasticity and functional recovery.

Editorial Notes:

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

About this neurology Research:

• Media Contact: SfN Media
• Source: SfN
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: The findings will be published in Journal of Neuroscience

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

 

Can your doctor rub a couple of neurons together and get human testing going? Or is sitting with heads up the ass the likely outcome?

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

Summary:

Researchers at UC San Diego have identified  (CST), a naturally occurring peptide fragment, that simultaneously reduces amyloid and tau buildup, quells neuroinflammation, and improves cognitive and motor performance in mouse models of neurodegenerative disease. Unlike single-target therapies, CST acts across several interconnected pathological pathways, pointing toward a versatile peptide-based treatment strategy for complex dementias.

Key Facts:

• Multi-Target Clearance: In preclinical mouse models, treatment with catestatin significantly reduced toxic accumulations of both tau and amyloid proteins while dialing down neuroinflammation.
• Functional Recovery: Beyond clearing hallmark neuropathology, the peptide led to measurable improvements in both cognitive performance and motor coordination in animal models.
• Derived from Chromogranin A: CST is an endogenous cleavage product of chromogranin A, a protein fundamental to neurotransmitter storage and cellular signaling, and is currently being explored for its ability to reprogram brain energy metabolism to shield vulnerable neurons against cellular stress.

Source: University of California San Diego School of Medicine

Alzheimer’s disease and related dementias present one of the most stubborn hurdles in modern neurology, primarily because their pathology is not driven by a single isolated defect. Instead, disease progression involves an entangled network of problems: aberrant protein aggregation, persistent neuroinflammation, metabolic dysfunction, and progressive synaptic failure.

While many experimental drugs focus narrowly on single targets, such as clearing amyloid plaques or blocking tau tangles, a research team at the University of California San Diego School of Medicine and the VA San Diego Healthcare System took a different approach. In a study published in Molecular Therapy, the scientists investigated whether an endogenous peptide could intervene across multiple disease mechanisms simultaneously.

Their focus fell on catestatin (CST), a naturally occurring peptide fragment derived from chromogranin A. In animal models, CST not only cleared pathological hallmarks but also protected functional neural circuits.

“Neurodegenerative diseases involve multiple interconnected problems — including misfolded proteins, neuroinflammation and progressive dysfunction of brain cells,” said senior author Sushil K. Mahata, PhD, professor of medicine at UC San Diego School of Medicine and research physiologist at the VA San Diego Healthcare System.

“Our findings show that CST can act across several of these disease-associated pathways and shift the brain toward a healthier state. More broadly, the study suggests that peptide-based therapies may offer a new approach to treating complex neurodegenerative diseases.”

Reducing Amyloid, Tau, and Neuroinflammation

To evaluate the peptide’s therapeutic potential, the investigators administered CST to mouse models displaying hallmark features of neurodegenerative decline. The treatment produced widespread structural and cellular benefits:

• Toxin Clearance: CST significantly blunted the accumulation of both amyloid and tau aggregates, the twin proteinopathies characteristic of Alzheimer’s disease.
• Anti-Inflammatory Modulation: The peptide suppressed chronic neuroinflammatory signaling, reducing destructive immune activation in brain tissue.
• Behavioral and Motor Gains: Mice receiving CST demonstrated meaningful improvements in memory, learning tasks, and motor performance compared to untreated controls.

Because chromogranin A is naturally involved in cellular communication and the packaging and release of hormones and neurotransmitters, its derivative CST already plays diverse roles across cardiovascular, metabolic, and immune regulation throughout the body. This native systemic versatility appears to translate to the central nervous system, where it orchestrates several defensive processes rather than engaging only one receptor.

Cellular Resilience and Metabolic Support

Beyond cleaning up cellular debris and cooling inflammatory fires, the researchers are examining how CST alters neuronal bioenergetics.

“One exciting aspect of our findings is that CST may do more than reduce the pathological features of neurodegeneration. We are also investigating whether CST can alter how the brain produces and uses energy, which may help neurons become more resilient to the cellular stress that occurs during neurodegeneration,” said lead author Suborno Jati, PhD, a postdoctoral scholar at UC San Diego School of Medicine.

By potentially stabilizing how distressed brain cells generate and utilize ATP, CST could give damaged neurons the energetic bandwidth required to maintain synaptic communication despite accumulating toxic stressors.

The Path Forward

The researchers emphasize that the current findings are strictly preclinical. Moving CST or related peptide analogues from laboratory animal models into human clinical trials will require comprehensive studies to determine long-term safety, optimal dosing regimens, blood-brain barrier delivery dynamics, and clinical efficacy.

Nevertheless, the discovery highlights the promise of peptide therapeutics as multi-system regulators capable of treating the multifaceted biology of neurodegenerative decline.

Funding: The research was supported in part by grants from the National Institutes of Health and the U.S. Department of Veterans Affairs.

Mahata is founder of CgA Therapeuticals, Inc. and co-founder of Siraj Therapeutics. Mahata and Jati are listed as co-inventors on intellectual property related to the findings.

Editorial Notes:

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

About this Genetics and Neuroregeneration Research:

• Media Contact: Miles Martin
• Source: UCSD
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Molecular Therapy (September 21, 2026). “Catestatin peptide ameliorates tauopathy and amyloidogenesis via adrenergic inhibition.” Authors: Suborno Jati, Satadeepa Kal, Daniel Munoz-Mayorga, Kechun Tang, Debashis Sahoo, Xu Chen, and Sushil K. Mahata.
• DOI: 10.1016/j.ymthe.2026.09.022

This type of brain training may actually cut your Alzheimer’s risk

 

My god, your doctor is IS SO FUCKING INCOMPETENT THERE STILL IS NO COGITIVE RECOVERY  PROTOCOL!

Meaning exact length of time and exact software to get! Which proves your board of directors is so incompetent they can't recognize crapola in their hospital that needs to be removed! YOU need to reconstitute the hospital!

cognitive speed training (20 posts to March 2014)

This type of brain training may actually cut your Alzheimer’s risk

Fact checked by Nick Blackmer

• Why this matters: Alzheimer’s disease affects millions and is expected to rise, making prevention crucial.
• What you can do: Engage in speed-based cognitive training exercises regularly.
• The payoff: Speed training can strengthen neural networks and lower Alzheimer’s risk.

Could games designed to strengthen mental skills help prevent Alzheimer’s disease as you age? According to a new 20-year study, they may.

More than 7 million Americans have Alzheimer’s disease, and that number is expected to rise to 13 million by 2050, according to the Alzheimer’s Association. There’s no proven way to prevent or cure the disease, but delaying its onset—even modestly—can help preserve and prolong people’s independence and quality of life. “That’s why expanding the menu of evidence-based prevention tools is so critical,” said Vernon Williams, MD, a sports neurologist and founding director of the Center for Sports Neurology and Pain Medicine at Cedars-Sinai Orthopaedics in Los Angeles.

How the Study Began

The new research, published in the medical journal Alzheimer’s & Dementia: Translational Research & Clinical Interventions, traces back to 1998. That’s when researchers recruited 2,802 older adults—most of whom were women and white—and assigned them to one of three groups receiving different forms of cognitive training or to a control group that received no cognitive training.

 Related video:  NIH-funded study finds midlife brain changes may help explain dementia risk (KYTX-TV Tyler-Longview)

 Participants in the cognitive training groups completed memory, reasoning, or speed-of-processing tasks during 10 sessions lasting 60 to 75 minutes over five to six weeks. The speed-of-processing tasks were designed to improve mental quickness and the accuracy of object identification.

Approximately half of those in the cognitive training group completed up to four additional “booster” sessions held 11 months and 35 months after the initial training course.

In 2016, the researchers shared their initial discoveries, finding that participants who completed the speed-of-processing brain training exercises had a 48% lower risk of developing dementia over 10 years.

What the New Findings Suggest

For their latest findings, the research team analyzed 20 years of Medicare data, spanning 1999 to 2019, to identify who was diagnosed with dementia. They found that those who had the speed training intervention had a substantially lower risk of developing Alzheimer’s and related dementias later in life.

Among those who completed the speed training and additional booster sessions, 40% were eventually diagnosed with dementia compared to 49% in the control group. Speed training was the only brain game associated with significantly lower chances of developing the cognitive condition.

As Jonathan Rasouli, MD, a neurosurgeon at Northwell Health’s Staten Island University Hospital, summarized, “older adults who engage in specific speed-based cognitive training exercises may have a substantially lower long-term risk of being diagnosed with Alzheimer’s disease, especially when booster training sessions are included.”

What’s the Takeaway?

Prior evidence shows that brain training exercises can improve cognitive performance in both the short and long term. But the new report “suggests that how we train the brain matters,” Williams said.

The fact that only speed training was linked to a lower risk of dementia is an important detail. Targeted, reinforced brain training may influence long-term dementia risk more than, say, isolated sessions. “Brain health requires the right stimulus, the right dose, and ongoing reinforcement with feedback,” Williams said.

Rasouli added that cognitive exercises that improve processing speed, divided attention, and rapid visual decision-making may strengthen neural networks and resilience. This could, in turn, help “the brain better account for age-related changes and reduce the chances of a dementia diagnosis decades later,” he explained.

That said, this doesn’t mean brain training is a magic bullet. “Cognitive training should be part of a holistic brain-healthy lifestyle, including physical exercise, sleep quality, social engagement, and diet,” Rasouli said.

Looking ahead, experts said more research is needed to understand who benefits most from brain training and how other preventative strategies, like exercise and sleep hygiene, can impact dementia risk when combined with brain training.

Read the original article on Health

A new study found a surprising anti-aging benefit in certain types of chocolate

 My god, your doctor is IS SO FUCKING INCOMPETENT THERE STILL IS NO CHOCOLATE PROTOCOL!

Meaning exact amounts and % cocoa! Which proves your board of directors is so incompetent they can't recognize crapola in their hospital that needs to be removed! YOU need to reconstitute the hospital!

dark chocolate (31 posts to March 2014)

A new study found a surprising anti-aging benefit in certain types of chocolate

Key Takeaways

• Dark chocolate’s theobromine may slow biological aging. A recent study found that theobromine—a compound abundant in dark chocolate—is linked to a longer lifespan and more favorable epigenetic aging markers.

• Theobromine stood out more than coffee-related compounds. While both cocoa and coffee contain beneficial metabolites, theobromine in chocolate had a stronger association with healthier aging compared to similar compounds like caffeine in coffee.
• Research suggests theobromine may support brain function, heart health, blood pressure, and gut health—though more studies are needed to confirm how it works in humans.

When you’re itching for a sweet treat, health experts will often tell you that dark chocolate is one of the best options to grab. But according to a recent study published by Aging-US, dark chocolate can do more than just satisfy your sweet tooth with minimal risk—it can also slow down biological aging thanks to its high levels of theobromine. 

The study surveyed 509 twin female participants, both monozygotic (identical) and dizygotic (fraternal), and monitored their metabolomic data and dietary intake. The study identified six metabolites from both cocoa (found in dark chocolate) and coffee, which included theobromine, caffeine, paraxanthine, 7-methylxanthine, and theanine. What they found was that theobromine is associated with an increased lifespan and epigenetic level.

The Link Between Theobromine and Longevity

Epigenetic deregulation, or the process by which genes turn “on” and “off,” plays a key role in how we age. “Multiple studies have developed epigenetic clocks towards predicting different age-related features, such as chronological age, time to death, pace of ageing, as well as other molecular biomarkers of ageing, including telomere length,” the study notes. “As such, epigenetic clocks may act as useful tools for assessing whether specific dietary phytochemicals are associated not only with epigenetic modifications, but also with the rate of aging, as measured by these clocks.” 

 Related video: Coffee and heart health (KXAN Austin) searchers used both as markers to identify a correlation. 

Since both cocoa and coffee contain theobromine, the researchers used both as markers to identify a correlation. During their sensitive analysis, they concluded that, compared to the metabolites found in coffee, theobromine had the highest association effect. For example, on a smaller scale, one study found that modest supplementation of theobromine in mice led to a significant increase in neurotrophic function (or essentially, how effectively the brain works). Even higher doses of the metabolite were associated with improved lipid profiles, lower blood pressure, and a healthier gut microbiome.

Further research even suggests that consumption of theobromine can be especially beneficial for smokers, who can improve their epigenetic age by quitting smoking and increasing their intake of theobromine. Theobromine can also enhance the vascular impact of flavanols, or plant compounds that are prevalent in cocoa. Although further research is needed to confirm theobromine’s many mechanisms, the study confirms that consumption of theobromine—including a healthy dose of dark chocolate—can contribute to an extended human lifespan.

Read the original article on Real Simple

Rhythm of Your Breath Controls Reaction Time

 Your competent? doctor created a breathing protocol years ago based on these books, right? 

Like:

'Breath: The New Science of a Lost Art' by James Nestor. Published 2020

Or;

'The Oxygen Advantage: Simple, Scientifically Proven Breathing Techniques to Help You Become Healthier, Slimmer, Faster, and Fitter' by Patrick McKeown. Published 2016

Or should you be doing fast breathing in

Creation of nitric oxide via Breath of Fire  February 2014 

And why doesn't your doctor know a damn thing about a breathing protocol?

Your doctor has had years to know about this. Are you giving them a pass on being incompetent? So, you DON'T have a functioning stroke doctor or hospital, do you?

Oh NO, INCOMPETENCE REIGNED, nothing doing! What do you do? Call the president and demand some competence in the hospital! That means EXACT 100% RECOVERY PROTOCOLS! 

Rhythm of Your Breath Controls Reaction Time

Summary:

Neuroscientists have discovered that human reaction speed changes across the respiratory cycle, with reaction times averaging 41 milliseconds faster during exhalation than inhalation. The study represents the first continuous measurement of cognitive response speeds across all breathing phases, including breath pauses, revealing that bodily rhythms actively modulate sensory-motor processing.

Key Facts:

• The Exhalation Advantage: Participants responded to unexpected visual stimuli an average of 41 milliseconds faster during exhalation than during inhalation, alongside a 21-millisecond advantage during post-breath pauses.
• Continuous Respiration Tracking: The investigation marks the first experiment to evaluate psychomotor vigilance continuously across all respiratory phases, linking airflow monitoring to millisecond-level motor outputs.
• Brain Oscillations Synchrony: Researchers suggest the effect is driven by neurophysiological efficiency, building on evidence that fundamental cortical oscillations naturally phase-lock with nasal breathing rhythms.

Source: Northwestern University

Whether an Olympic swimmer reacts to the crack of a starting pistol or a highway driver slams on the brakes to avoid an oncoming crash, a fraction of a second often determines victory, defeat, or survival. At 60 mph, a car travels nearly four feet in just 40 milliseconds, a brief window of time where sensory processing speed is paramount.

Now, a study led by neuroscientists at Northwestern University reveals that this critical response margin is tied directly to the rhythm of our lungs.

Published in iScience, the research demonstrates that human response times fluctuate reliably across the breathing cycle. When presented with rapid visual prompts, people react significantly faster when exhaling than when inhaling, establishing a functional bridge between autonomic respiratory mechanics and conscious motor readiness.

“By using a tangible and easy to understand task, we were able to show the relationship between respiration and cognition, which I hope people in a range of fields will find application for,” said lead author Erika M. Yamazaki, Ph.D., a neuroscientist and former member of Northwestern’s Cognitive Neuroscience Laboratory. “Study of the brain and body connection is still a new field of research, which makes the study findings all the more exciting.”

Mapping Psychomotor Vigilance Across Breaths

To measure how breathing modulates executive reflexes, the researchers recruited 35 healthy adult participants aged 18 to 33 to perform the Psychomotor Vigilance Task (PVT)—a standard clinical and cognitive measure of sustained attention and reaction latency.

During the assessment, participants monitored a display screen and pressed the space bar as rapidly as possible whenever a red square turned yellow. Throughout the trials, subjects wore a nasal cannula-style airflow sensor positioned directly under their nostrils to capture real-time respiratory phases with high temporal resolution. Each participant completed testing protocols twice: once before and once after an in-lab sleep period (either a daytime nap or an eight-hour overnight rest).

By correlating thousands of millisecond-level key presses with simultaneous airflow waveforms, the team identified distinct performance variations:

• Exhalation vs. Inhalation: Motor responses during active exhalation were an average of 41 milliseconds (approximately 1/25th of a second) faster than responses executed during active inhalation.
• Breath Pauses: The brief periods of breath retention between inhalation and exhalation also maintained an advantage, clocking in 21 milliseconds faster than inhalation phases.

“This study documents an important link between respiration and the brain systems for responding to environmental events,” said senior author Ken Paller, Ph.D., the James Padilla Professor of Psychology at Northwestern University. “We don’t yet know exactly how they are linked, but we suspect neurophysiological efficiency, because other studies have shown that various brain oscillations are synchronized with the rhythms of one’s breathing.”

Respiratory Phase-Locking and Sleep Engineering

The finding aligns with growing neuroimaging evidence showing that nasal respiration entrains slow-wave neural oscillations across diverse brain networks, including the olfactory bulb, piriform cortex, amygdala, and hippocampus. During inhalation, sensory inputs and emotional memory consolidation undergo specific neural gating; during exhalation and baseline pauses, cortical networks may optimize motor preparation pathways.

Beyond optimizing athletic reaction starts or high-speed driving reflexes, the researchers emphasize that mapping the respiration-cognition axis has crucial clinical implications for sleep medicine.

Paller’s laboratory is currently expanding on these findings through an NIH-funded initiative led by Yamazaki that explores the cognitive fallout of obstructive sleep apnea, a widespread, underdiagnosed condition where repeated breathing cessations fragment sleep architecture and erode next-day mental capacity.

By detailing how respiratory rhythms modulate cortical activity during both waking and resting states, the investigators aim to pioneer noninvasive “sleep engineering” techniques that stabilize breathing patterns and preserve long-term cognitive health.

Editorial Notes:

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

About this Cognitive Neuroscience Research:

• Media Contact: Stephanie Kulke
• Source: Northwestern University
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: iScience (Sept 22, 2026). “Response speed is modulated by respiratory phase.” Authors: Erika M. Yamazaki and Ken A. Paller.
• DOI: 10.1016/j.isci.2026.117535

7 Supplements That Actually Have Healthspan Research Behind Them by Super Age

 Your competent? doctor better have protocols on these already! 

NO, So PURE INCOMPETENCE and hasn't been fired yet?

Board of directors incompetence in full display in not getting recovery protocols created!

7 Supplements That Actually Have Healthspan Research Behind Them

Beneficial effects of eight weeks of FES-assisted cycling on aerobic capacity and paretic quadriceps thickness in post-stroke hemiparesis

 'Improved' IS STILL FAILURE! It means your competent? doctor and hospital has lots more work to do to get to 100% recovery! Make sure you DEMAND 100% RECOVERY PROTOCOLS from your doctor! Nothing less!

Beneficial effects of eight weeks of FES-assisted cycling on aerobic capacity and paretic quadriceps thickness in post-stroke hemiparesis

• Maël Descollonges,
• Julie Di Marco,
• Pierre-Henri Pouillart,
• Ehsan Jafari,
• Lana Popović-Maneski,
• Ana Z. Radić,
• Olivera C. Djordjević,
• Ljubica M. Konstantinović,
• Sindi Z. Mitrović,
• Julien V. Brugniaux &
• Gaëlle Deley 

• 43 Accesses

• Explore all metrics

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.

Abstract

Background

Stroke is a leading cause of long-term disability worldwide, frequently impairing walking ability, postural control, and muscle strength. Hemiparesis, affecting nearly 90% of stroke survivors, results in unilateral motor deficits and presents substantial rehabilitation challenges. Functional electrical stimulation-assisted cycling (FES-assisted cycling) has shown potential to activate paretic muscles, improve aerobic capacity, and enhance motor coordination.

Objective

This study aimed to compare the effects of an 8-week FES-assisted cycling program (Kurage, Lyon, France) versus traditional cycling (without stimulation) on aerobic fitness, muscle thickness, and walking performance in post-stroke participants.

Methods

This randomized study included 31 post-stroke participants (21 men, 10 women; age: 57 ± 12 years), who were randomly assigned to either an FES-assisted cycling group or a conventional cycling group. Both groups completed 24 cycling sessions (30 min each) over 8 weeks, in addition to standard rehabilitation. Outcomes included peak oxygen uptake (V̇O₂peak), maximal power output, muscle thickness (rectus femoris and vastus intermedius), and walking ability (6-Minute and 10-Meter Walk Tests).

Results

Both groups showed significant improvements in V̇O₂peak, power output, muscle thickness, and walking test performance. The FES group showed greater gains in V̇O₂peak (+ 27% vs. +12% in the control group; P = 0.038) and in paretic muscle thickness (rectus femoris: +17% vs. +3%, P = 0.036; vastus intermedius: +24.6% vs. +7%, P = 0.029). A trend toward greater improvement in the 6-Minute Walk Test was also observed in the FES group (+ 43% vs. +25%; P = 0.082).

Conclusion

FES-assisted and traditional cycling improved exercise capacity, muscle thickness, and walking ability in post-stroke participants. FES-assisted cycling led to additional benefits specifically for V̇O₂peak and localized hypertrophy in the paretic muscles targeted by FES, suggesting specific neuromuscular adaptations that are not commonly described in previous studies. These peripheral changes indicate that FES-assisted cycling may offer unique muscular benefits, particularly for individuals with limited voluntary control. These findings refine our understanding of FES as a complementary tool in stroke rehabilitation. Further research with larger cohorts and longer follow-up is needed to confirm these effects and assess long-term outcomes.