Cancer Drug Halts Fragile Brain Bleeds

 Hopefully your competent? doctor has been working on solving CCMs for over 6 years. 

NO? So, PURE INCOMPETENCE displayed then?

Cerebral Cavernous Malformation (2 posts to September 2020)

Cancer Drug Halts Fragile Brain Bleeds

Summary:

Researchers have discovered that dabrafenib, an FDA-approved BRAF inhibitor currently prescribed for pediatric brain tumors, significantly reduces the size and number of vascular malformations in Cerebral Cavernous Malformation (CCM). By screening over 5,000 bioactive molecules, the team demonstrated that dabrafenib suppresses vessel leakage, normalizes vascular architecture, and prevents hemorrhagic progression in animal models, offering a viable drug-based alternative to invasive brain surgery.

Key Facts:

• Drug Repurposing Breakthrough: High-throughput screening of more than 5,000 compounds identified dabrafenib, an established treatment for pediatric low-grade glioma, as an effective therapeutic agent against CCM.
• Dual-Pathway Targeting: Dabrafenib selectively inhibits two aberrant molecular signaling pathways driving cavernoma growth, successfully shrinking vascular lesions and halting lesion formation in vivo.
• Vessel Stabilization and Leakage Suppression: Beyond reducing lesion volume and burden, the drug restored vascular integrity, curbed cerebral microhemorrhages, and repaired vascular defects in the retina.

Source: Uppsala University / SciLifeLab

Cerebral Cavernous Malformation (CCM) is a devastating vascular condition characterized by the formation of fragile, mulberry-like clusters of dilated capillaries within the central nervous system. Because the walls of these malformed vessels lack proper structural integrity and endothelial tight junctions, they are prone to chronic micro-leakage and catastrophic intracranial hemorrhages, often leading to neurological deficits, seizures, and hemorrhagic strokes.

To date, no approved pharmacological therapy exists for CCM. The only available clinical intervention is neurosurgical resection, an invasive option fraught with surgical risks and frequently unfeasible for patients who present with multiple deep-seated or brainstem lesions.

Now, a collaborative study led by researchers at Uppsala University and SciLifeLab reveals a non-invasive therapeutic candidate.

Publishing their preclinical findings, the team discovered that dabrafenib, a targeted BRAF inhibitor already approved by the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for pediatric brain tumors, effectively halts cavernoma progression, stabilizes leaky vessels, and shrinks pre-existing vascular malformations.

High-Throughput Screening Identifies a Dual-Action Inhibitor

To find therapeutic molecules capable of reversing CCM pathology, the researchers conducted an unbiased screening campaign assessing more than 5,000 bioactive compounds against cultured CCM mouse vascular endothelial cells.

The primary objective was identifying candidates capable of reverting the chaotic, destabilized endothelial phenotype back to a healthy state. The most promising lead was dabrafenib.

“We tested more than 5,000 bioactive molecules on cultured CCM mouse vascular cells to identify compounds that could normalise their pathogenic phenotype. Top drug candidates were subsequently studied in cultured human brain vascular cells and in CCM animal models,” explained first and co-corresponding author Maximiliano Arce. “The most promising results came from dabrafenib, a BRAF inhibitor that efficiently reversed the pathological phenotype in vitro and halted cavernoma progression in vivo. Remarkably, dabrafenib targeted two pathological signalling pathways that contribute to CCM development and progression.”

Sealing the Blood-Brain Barrier and Shrinking Lesions

Following initial cellular validation in human brain microvascular cells, the team evaluated dabrafenib’s efficacy in genetic mouse models of CCM.

The in vivo results demonstrated substantial therapeutic benefits across multiple parameters:

• Lesion Regression: Oral administration of dabrafenib produced a marked reduction in both the overall number and physical volume of brain cavernomas.
• Leakage Suppression: The drug stabilized the fragile endothelial lining, halting the vascular permeability and micro-hemorrhages that cause clinical neurological deterioration.
• Retinal Rescue: Dabrafenib also resolved abnormal vascular remodeling in the retina, a secondary clinical manifestation observed in many CCM patients.

Accelerating Clinical Translation

Because bringing a de novo pharmaceutical compound through preclinical design and Phase I safety trials typically spans over a decade, repurposing an established drug offers a critical shortcut for patients living under the constant threat of brain bleeds.

Dabrafenib is already widely utilized in pediatric oncology to manage BRAF-mutated low-grade gliomas, meaning its pharmacokinetic behavior, dosage tolerance, and human safety profile are well documented.

“Since dabrafenib is already approved by the U.S. Food and Drug Administration and the European Medicines Agency, and has an established safety profile, it represents a strong candidate for rapid clinical translation to halt brain cavernoma growth and progression,” said senior author Peetra Magnusson.

The research consortium, which worked in close collaboration with the SciLifeLab BioImage Informatics Unit to quantify vascular architectures, is now laying the groundwork for clinical trials to evaluate dabrafenib’s efficacy in human patients with familial and sporadic CCM, aiming to replace neurosurgery with targeted precision pharmacotherapy.

Editorial Notes:

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

About this neurotech and schizophrenia Research:

• Media Contact: Sandra Gunnarsson
• Source: Uppsala University
• Image Credit: Image credited to Maximiliano Arce
• Original Research is Open Access: Science Translational Medicine (Oct 1, 2026). “The kinase inhibitor dabrafenib halts progression of cerebral cavernous malformations in a BRAF-independent manner.” Authors: Maximiliano Arce, Hua Huang, Charlotte Rorsman, Iza Erzar, Joppe Oldenburg, Ying Sun, Ross Smith, Favour C. Onyeogaziri, Stefano Barbera, Frida C. Ahlstrand, Petter Ranefall, Anna Klemm, Mark Richards, Anna Dimberg, Lena Claesson-Welsh, and Peetra U. Magnusson.
• DOI: 10.1126/scitranslmed.adr0448

Automated quantification of movement qualities in the human upper extremity after stroke using a wearable robot

 Nothing here gets survivors recovered! You need EXACT PROTOCOLS for that! Complete failure of the mentors and senior researchers supervising!

'Assessments' have never gotten anyone recovered!

Automated quantification of movement qualities in the human upper extremity after stroke using a wearable robot

• Yoon No Gregory Hong,
• Kyoungsoon Kim,
• Sheng Li,
• Marcia K. O’Malley,
• Ashish D. Deshpande &
• Jinsook Roh 

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 adult disability, with approximately 80% of survivors experiencing upper extremity (UE) motor impairments. Clinical assessment tools like the Fugl-Meyer Assessment (FMA) are widely used but limited by ordinal scales and subjective observation. While rehabilitation robots offer high-resolution data, their clinical translation is hindered by a lack of standardized protocols and limited interpretability for clinical decision-making.

Objective

This study aimed to develop an objective, standardized, and clinically interpretable assessment tool to quantify UE motor qualities by integrating exoskeleton technology with traditional clinical assessment tasks.

Methods

Ten healthy individuals and ten stroke survivors performed seven standardized tasks (six from the FMA-UE and one additional elbow task) while wearing the HARMONY exoskeleton. We developed a “trajectory pattern discrepancy score” based on the root mean square error between individual joint trajectories and normative averages. Additionally, kinematic synergy analysis was performed using non-negative matrix factorization to evaluate alterations in multi-joint coordination.

Results

The trajectory pattern discrepancy score showed a strong negative correlation with clinical FMA-UE scores (r = -0.93, p < 0.01) and demonstrated excellent test-retest reliability (ICC = 0.98). The number of identified kinematic synergies decreased significantly as motor impairment severity increased (r = 0.79, p < 0.01). Furthermore, kinematic synergy analysis provided a mechanistic explanation for reduced individual joint control. Post-stroke synergies could be explained through the merging (linear combinations of healthy kinematic patterns), preservation, or loss of healthy kinematic synergies, reflected as pathological joint coupling and loss of specific individual joint control.

Conclusions

This study presents a novel, standardized assessment framework that integrates exoskeleton technology with conventional clinical tasks. By bridging the gap between objective robotic data and clinical interpretability, this approach would enable robust motor impairment assessment and intuitive phenotyping of motor characteristics to guide personalized rehabilitation strategies.

Doing This May Lower Blood Pressure More Than a Workout

 Along with this your competent? doctor told you about all the benefits of heat shock proteins, right?

• heat shock proteins (12 posts to April 2013)

NO? So, fucking incompetence exists in your doctor and hospital? And the board of directors is so incompetent they can't recognize incompetence in their own hospital! Time to reconstitute the hospital! 

Doing This May Lower Blood Pressure More Than a Workout

According to a study published in the European Journal of Applied Physiology, a nice, relaxing hot bath is genuinely relaxing enough that it might lower your blood pressure more than an intensive 30-minute workout.

Researchers at the University of Western Australia gathered 25 overweight or obese adults aged 45 to 70 and subjected them to two distinct tests, spaced at least three days apart. In one session, participants spent 30 minutes chest-deep in a tub of 104°F water. In the other, they spent 30 minutes pedaling on a stationary bike at a moderate pace.

When scientists scanned the tiny blood vessels beneath the participants’ skin using optical coherence tomography, the tub beat the bike across the board. Turning a bathtub into a you-flavored soup caused bigger increases in blood vessel diameter and blood flow speed, along with more overall microvascular density than pedaling a bike.

That 30-minute soak even produced slightly larger drops in both systolic and diastolic blood pressure, which you might otherwise know as the numerical values after getting your blood pressure checked.

Your Evening Bath Could Have a Benefit Beyond Relaxation

The idea here is that when your core body temperature goes up when you’re soaking in a hot tub, your circulatory system enters a kind of overdrive state in an attempt to dissipate heat, thereby dilating blood vessels through a process called vasodilation, surging blood through your skin. When you’re on a bike, your heart rate spikes due to muscle contraction, but your blood vessels are experiencing the same kind of extreme thermal strain.

None of this means that you should replace your cycling routine with a tub soak, since the benefits of a hot bath versus cycling begin and end at lowering blood pressure. When you’re exercising, you’re building muscle and burning calories, all while strengthening your heart, all stuff that a bath will never be able to replicate.

If you’re young, pedal away and then soak in a hot bath for 30 minutes afterward if you really want to get your blood pressure down. Older adults and anyone dealing with mobility issues can turn to a steaming hot bath to reap the apparently legitimate low-effort blood pressure benefits.

Neuroplasticity Biomarkers and Neurotransmitter Modulation in Post-Ischemic Stroke Rehabilitation: A Narrative Review

 You know nothing about how to make neuroplasticity repeatable on demand, so a useless word salad!

When your incompetent? doctor/researcher uses this word ask them to EXPLAIN EXACTLY what needs to happen for a neuron to drop a current task and take on a neighbors! 

NO explanation; PURE FUCKING INCOMPETENCE! Not knowing that makes neuroplasticity non repeatable on demand!

Neuroplasticity Biomarkers and Neurotransmitter Modulation in Post-Ischemic Stroke Rehabilitation: A Narrative Review

-Ischemic Stroke Rehabilitation: A Narrative Review

,

,

and

1

Department of Neurology, Dr. K. Jonscher Muncipal Medical Centre in Lodz, Milionowa 14, 93-113 Łódź, Poland

2

Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Łódź, Poland

3

Department of Neurological Rehabilitation, Medical University of Lodz, Milionowa 14, 93-113 Łódź, Poland

*

Authors to whom correspondence should be addressed.

J. Clin. Med.2026, 15(20), 8091;https://doi.org/10.3390/jcm15208091

This article belongs to the Special Issue Cerebrovascular Disease: Symptoms, Diagnosis and Current Treatment—Second Edition

Version Notes

Order Reprints

Abstract

Background/Objectives: 

Recovery after stroke is a complex process involving structural and functional reorganization of the nervous system. Neuroplasticity plays a key role in functional recovery, while biomarkers and neurotransmitter systems may reflect or modulate the biological processes underlying rehabilitation and adaptation after stroke. The aim of this review was to summarize the current evidence regarding biomarkers of neuroplasticity and neurotransmitter modulation in post-stroke rehabilitation, with a particular focus on their potential importance for functional recovery and rehabilitation outcomes. 

Methods: 

This narrative review synthesized evidence identified through searches of PubMed/MEDLINE, Scopus, and Web of Science, supplemented by reference-list screening. The literature was qualitatively analyzed according to the main themes of the review. 

Results: 

Current data point to BDNF, VEGF, and MMPs as promising biomarkers associated with post-stroke neuroplasticity and functional recovery. Neurotransmitter modulation, particularly involving GABA, glutamate, dopamine, and serotonin, may influence neuronal excitability, synaptic plasticity, and motor learning after stroke. The combination of biomarker assessment and rehabilitation-based modulation of these pathways may provide a more comprehensive approach to understanding and monitoring post-stroke recovery. 

Conclusions: 

Current evidence supports the role of neuroplasticity-related biomarkers and neurotransmitter modulation as potential tools for understanding biological responses to post-stroke rehabilitation. However, their clinical relevance and usefulness in guiding individualized rehabilitation require further validation in future clinical studies.

Application of artificial intelligence in the prediction and management of stroke rehabilitation

 Putting three useless items for stroke in one research paper has got to be the PINACLE OF STUPIDITY!

• Artificial intelligence doesn't do any good until the underlying exact protocols for recovery exist!
• Predictions DO NOTHING FOR DELIVERING RECOVERY!
• Management does nothing useful!

Application of artificial intelligence in the prediction and management of stroke rehabilitation

Stroke is a major cause of long-term disability, and recovery varies substantially across motor, cognitive, communication, and activities-of-daily-living domains, making continuous assessment and individualized rehabilitation essential. However, current rehabilitation decisions still rely heavily on periodic clinical scales, clinician experience, and local resources, which may not fully capture differences in lesion characteristics, baseline function, comorbidities, and recovery trajectories. Access is also limited by geographic barriers, uneven service capacity, and intermittent follow-up. Artificial intelligence is increasingly being explored for stroke imaging, early prognosis, rehabilitation-outcome prediction, movement and physiological assessment, robot- and virtual-reality-assisted training, brain–computer interfaces, wearable monitoring, and telerehabilitation, offering new opportunities for more adaptive and continuous care. “Yet acute diagnosis, early prognostication, and rehabilitation-specific outcomes are often discussed together despite addressing different clinical questions, and many rehabilitation applications remain supported mainly by small datasets, internal validation, or early feasibility studies. Technical performance therefore should not be equated with rehabilitation benefit.” said the author Weihua Song, a researcher at Capital Medical University, “This creates a need for a structured review that maps AI applications to their clinical decision points, rehabilitation relevance, validation maturity, and readiness for clinical translation.”

This study used a structured narrative review design, systematically searching PubMed/MEDLINE, IEEE Xplore, Web of Science, and Scopus for studies on artificial intelligence and stroke rehabilitation published from January 2010 to March 2025, with a PRISMA-style process used to improve transparency. The database searches identified 1,247 records, and after deduplication, title and abstract screening, and full-text assessment, 108 publications were included in the thematic synthesis. The reviewers extracted information on study design, AI technique, sample size, rehabilitation domain, outcomes, model performance, validation methods, and reported limitations. Evidence was organized into four major themes: AI for rehabilitation-outcome prediction, rehabilitation assessment and monitoring, therapeutic intervention and management, and integration of AI with robotics, virtual reality, brain–computer interfaces, wearable technologies, and telerehabilitation. Importantly, the review distinguishes acute diagnostic or prognostic evidence from rehabilitation-specific outcomes and evaluates each application according to validation quality, clinical relevance, and implementation barriers

One of the major applications of artificial intelligence in stroke rehabilitation is the prediction of subsequent functional recovery using clinical scales, imaging, EEG, wearable-sensor data, and demographic information. Existing studies have explored prediction of 90-day functional status, changes in Barthel Index, motor-function scores, language and cognitive recovery, quality-of-life improvement, and long-term mortality, using machine learning, deep learning, and explainable models to identify factors associated with recovery trajectories. Acute imaging and early prognostic models can provide baseline information on lesion burden, initial severity, and treatment response that may inform later rehabilitation planning, whereas rehabilitation-specific prediction focuses more directly on changes in motor function, activities of daily living, participation, and patient-reported outcomes over time. However, most studies remain retrospective, small, or single-center and rely mainly on internal validation, while independent multicenter external validation and prospective clinical-impact studies are still uncommon. Therefore, strong predictive accuracy indicates potential for risk stratification, but does not by itself demonstrate that AI-guided treatment improves rehabilitation outcomes.

Artificial intelligence is increasingly being used to automate the assessment and continuous monitoring of motor function, posture, gait, and rehabilitation progress after stroke, complementing conventional clinical scales and periodic follow-up. Existing systems combine EEG, EMG, wearable sensors, motion tracking, and home-monitoring data to quantify movement patterns, exercise quality, and functional changes, while machine learning can identify abnormal movements or estimate clinical motor scores. Wearable and remote-monitoring technologies can further extend assessment into the home, providing longitudinal information on rehabilitation adherence and progression. However, many studies still focus primarily on technical feasibility, classification accuracy, or short-term surrogate outcomes, and commonly involve small samples, single-center datasets, and limited independent external validation. Heterogeneity in devices, data formats, and assessment schedules also restricts generalizability. Future work should therefore establish more standardized outcome measures and data pipelines and use multicenter, long-term, prospective studies to determine whether AI-based monitoring can meaningfully improve rehabilitation decisions and patient outcomes.

Beyond prediction and monitoring, artificial intelligence is increasingly being explored to support rehabilitation adjustment and the coordinated use of assistive technologies after stroke. Current approaches aim to adapt training intensity, task difficulty, and feedback frequency according to motor performance, cognitive status, and sensor-derived information, while integrating AI with rehabilitation robots, virtual reality, brain–computer interfaces, wearable devices, and telerehabilitation platforms. Robotic systems can provide standardized assisted movement, virtual reality emphasizes interactive task practice and augmented feedback, and BCIs can use neural signals to control external feedback or assistance when voluntary movement is severely limited. However, these technologies currently function mainly as rehabilitation adjuncts, with much of the evidence coming from small samples, short follow-up, and exploratory or single-arm studies; convincing evidence of superiority over conventional rehabilitation remains limited. A key future direction is the development of patient-centered closed-loop systems in which EEG, EMG, and wearable-sensor signals dynamically adjust robotic assistance, extended-reality tasks, and remote feedback while maintaining clinical supervision, interoperability, affordability, and compatibility with routine rehabilitation workflows.

Despite the growing potential of artificial intelligence for stroke rehabilitation prediction, assessment, and assisted intervention, clinical translation remains constrained by challenges in data, modeling, and implementation. Rehabilitation datasets are often small, heterogeneous, and inconsistently sampled, while multimodal clinical and sensor data remain difficult to standardize, increasing the risk of overfitting and limiting cross-institutional generalizability. In addition, the “black-box” nature of complex models can reduce clinical interpretability and trust, and improved predictive accuracy alone does not guarantee better treatment decisions or patient outcomes. Wearable monitoring, home rehabilitation, and remote-care platforms also raise concerns regarding privacy, security, data sharing, and device reliability. Future research should emphasize multicenter external validation and prospective clinical trials while developing genuinely closed-loop rehabilitation systems that combine clinical information, imaging, EEG, EMG, and wearable-sensor data to dynamically adjust robotic assistance, extended-reality training, and remote feedback. “Greater attention to explainability, interoperability, cost-effectiveness, and fairness will also be essential, with AI positioned as an adjunct to multidisciplinary care rather than a replacement for clinicians.” said Weihua Song.

Authors of the paper include Weihua Song, Shuai Si, Yinghui Wang, Hong Chang, and Xiaoying Tang.

This work was supported by the National Science and Technology Major Project (2023ZD0503800 and 2023ZD0503803), the Capital’s Funds for Health Improvement and Research (2024-1-2011), the Key R&D Program of China (2023YFC3605200 and 2023YFC3605201), the Project for Innovation and Development of Beijing Municipal Geriatric Medical Research Center (No. 11000025T000003320658), the Beijing “Young Seedling Program” for High-Level Innovative and Entrepreneurial Leading Talents (No. 2-1-008-0260), and the 2023 Special Nursing Project of Xuanwu Hospital, Capital Medical University (HLZD2023002).

The paper, “Application of Artificial Intelligence in the Prediction and Management of Stroke Rehabilitation” was published in the journal Cyborg and Bionic Systems on Oct 8, 2026, at https://doi.org/10.34133/cbsystems.0702.

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Journal

Cyborg and Bionic Systems

This Common Eating Habit Was Linked To 30% Lower Odds Of Frailty by mindbodygreen

 Will your competent? doctor GUARANTEE  this gets into your diet protocols(both hospital and home)?

This Common Eating Habit Was Linked To 30% Lower Odds Of Frailty

Scientists uncover a sleep-brain connection that could be the key to halting cognitive decline

 Your incompetent? doctor missed this well over a decade ago, right? Why don't you get them fired? There are no excuses for such massive incompetence!

Hormone Shots Aid Cognition in Older Adults August 2012

Scientists uncover a sleep-brain connection that could be the key to halting cognitive decline

The study monitored and recorded the brain activity of mice through electrode brain implants. Researchers stimulated neurons located in the hypothalamus, including the growth-hormone-releasing hormone (GHRH) neurons and two types of somatostatin neurons responsible for the regulation of the growth hormone release during the sleep-wake cycle. 

Once those hormones are released, they increase activity in the brainstem region that affects attention, arousal, and cognition. This region, called the locus coeruleus, has also been associated with several neurological and psychiatric issues, such as PTSD and depression. 

In this study, researchers found that GHRH stimulates growth hormone release while somatostatin suppresses it, essentially functioning like an accelerator and brake system in the brain. They also discovered that these peptides behave differently in REM and non-REM sleep states. During a non-REM state, somatostatin levels dropped while GHRH activity rose, promoting growth hormone release. “This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness,” said Daniel Silverman, a postdoctoral fellow at UC Berkeley and a co-author of the study.

Eventually, this finding could help researchers better understand and potentially develop treatments for various conditions, including sleep disorders, degenerative diseases like Parkinson’s and Alzheimer’s, and even metabolic conditions like diabetes.

“Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair, and metabolic health,” Silverman said. 

This post originally appeared at inc.com.

Who is more prone to Alzheimer’s? Scientists might have found a clue

 

With your risk of dementia post stroke, what will your competent? doctor do with this to prevent those problems? 

Parkinson’s Disease May Have Link to Stroke March 2017 

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

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

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

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Oh, sorry; NOTHING AT ALL! In my opinion your doctor is completely incompetent in not using research to get you recovered!

Who is more prone to Alzheimer’s? Scientists might have found a clue

A slight difference in DNA could shape some peoples’ susceptibility to developing Alzheimer’s disease, researchers have found.

Experts based at various institutions in Hong Kong found that Chinese participants with longer repeats of a specific gene sequence in their DNA were more likely to have the disease. The association was also noted among European participants, although it was much weaker.

The study was published in the journal Nature Neuroscience on October 12.

Researchers have previously identified several genetic variants that are believed to be associated with Alzheimer’s risk, and it is understood that those who have a parent or sibling diagnosed with the disease are more likely to develop it than people without those links—although this doesn’t mean that person will develop Alzheimer’s, it only increases the odds.

That said, Alzheimer’s does not have a single genetic cause, and is believed instead to be influenced by a combination of genetic, lifestyle and environmental factors.

What the experts set out to understand in this study was whether repeats of certain genetic sequences—rather than specific genetic variants—could influence risk.

Rudolph Tanzi, a professor of neurology at Harvard University, told Newsweek that the “potentially important” study “goes beyond the normal single-base genome variants that are tested in the many genome-wide association studies of Alzheimer’s disease.”

 Related video: New study identifies possible early sign of dementia (Welltica+)

“We know that the common DNA variants that show association with Alzheimer’s in genome-wide association studies account for less than 50 percent of the heritability of Alzheimer’s disease. So finding these types of DNA repeat variants in the genome is very important,” he said.

Dr. Michael Guo, an assistant professor of neurology and genetics, and a clinician in the University of Pennsylvania Memory Center, told Newsweek: “This is an exciting study that highlights the importance of studying diverse populations and expanding our analyses to include broader sets of spelling errors in our DNA.”

“Their work may help improve our ability to predict Alzheimer’s disease risk,” he added. “Ultimately, by identifying a new gene linked to Alzheimer’s disease, this could spur further work into how FAM193B causes disease and whether it may serve as a drug target.”

A Chinese cohort of over 3,000 people were included in the study—around half of whom had Alzheimer’s disease—as well as genetic data and records obtained from UK Biobank (around 2,600 with Alzheimer’s and almost 23,000 controls) to see whether the findings were the same among different ancestries.

From 11 of the Chinese participants, the researchers built a more detailed reference of different structural DNA sets and then analyzed the collections of the other DNA readings.

They noticed that the CCG DNA string could have repeats from between four to 30 among the participants, and found that those with at least 18 repeats had twice the odds of having Alzheimer’s disease than those with no more than 11 repeats. This indicates that repeated strands of the sequence could increase likelihood of having the disease, not a person’s lifetime risk of developing the disease.

The finding was also weaker—though still identified—among the European participants’ records from UK Biobank, meaning that the estimate among the Chinese cohort cannot be translated directly across different ancestral groups.

“This isn’t unexpected, many genetic variants including APOE have different effect sizes in populations of different ancestries,” Michael Lutz, a professor of neurology and pathology at Duke University, told Newsweek. APOE is the gene that has been associated with Alzheimer’s, and its variant APOE4 is the strongest known genetic risk factor for the disease.

What’s Behind The Association?

Reasons for this association could be down to FAM193B expression. The experts found that more repeats of the CCG sequence resulted in higher FAM193B expression, and that increased activity was separately found to result in nerve cell DNA damage and cellular harm.

The researchers also noted that FAM193B protein “directly interacts” with the enzymes GSK3alpha and GSK3beta, which is notable as they said when these enzymes dysregulate it can result in increased beta-amyloid and tau—the two proteins associated with Alzheimer’s disease.

“Analyses of postmortem human brains and cultured neuronal cells showed that elevated neuronal FAM193B expression is associated with DNA damage and cell death-related pathways which are key pathways involved in Alzheimer’s disease pathophysiology,” Lutz said.

“These findings establish the common FAM193B-CCG repeat as an Alzheimer’s disease risk genetic factor and highlight the contribution of common structural variants to Alzheimer’s disease heritability,” he added.

The experts emphasized that this does not mean that longer repeats of CCG damage neurons for certain or explain the association entirely.

What This Means For Alzheimer’s

Lutz said that it is “early to consider the impact of the findings on Alzheimer’s disease prevention and treatment,” but that the “most immediate application of the finding would be for Alzheimer’s disease risk prediction.” This is because the paper provides “support that including the structural variant, with the caveat of ancestral-specific risk, will improve lifetime disease risk prediction in clinical settings.”

He added that “as is pointed out in the paper, the biological function of the FAM193B gene is unclear, so further research would be needed to understand the biochemical and physiological impact of the repeat.”

Tanzi also said that the CCG variant association was found in a “relatively small Chinese population and will need to be replicated in larger populations.”

He added that the gene implicated here is “very interesting as one can imagine how it might affect tau tangle pathology downstream of amyloid deposition (by affecting the enzyme GSK3beta).”

“Functional studies along these lines are now warranted as well as replication of the genetic association with Alzheimer’s disease in larger populations,” he said.

Reference

Cao, H., Fu, Y., Zhou, X. et al. (2026) Genome-wide analysis of common structural variants in Alzheimer’s disease identifies a risk-associated regulatory CCG repeat in FAM193B. Nature Neuroscience. https://doi.org/10.1038/s41593-026-02481-z

Contact Newsweek editors on this story: Kara Dolman and Tony Phillips.

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Psilocybin Tied to Lower Inflammation in Parkinson's Trial

 Is your competent? doctor ready with this to try to prevent Parkinsons after your stroke? Sorry, your doctor doesn't even know of your Parkinson's risk! 

Parkinson’s Disease May Have Link to Stroke March 2017 

Haven't you gotten that INCOMPETENT DOCTOR FIRED YET?

Isn't your doctor already prescribing psilocybin for stroke recovery? Oh NO, you DON'T have a functioning stroke doctor, do you? 

psilocybin (59 posts to May 2014) 

Psilocybin Tied to Lower Inflammation in Parkinson's Trial

Key Takeaways

• Psilocybin therapy was associated with reduced inflammation in a small trial of Parkinson's patients with mood dysfunction.
• An inflammatory index remained lower through 30 days, but mitochondrial stress marker reductions were transient.
• Findings require confirmation in larger randomized controlled trials.

Markers of systemic inflammation and mitochondrial stress were reduced after psilocybin therapy in Parkinson's disease patients with mood dysfunction, a small nonrandomized trial showed.

Relative to baseline, an inflammatory index was significantly lower at all follow-up time points after psilocybin was administered, reported Ellen Bradley, MD, of the University of California San Francisco (UCSF), and co-authors.

The standard mean difference (SMD) was -0.72 (adjusted P=0.003) 1 day after 10 mg of psilocybin, Bradley and colleagues wrote in a JAMA Psychiatry research letter.

One day after 25 mg of psilocybin, the SMD was -0.60 (adjusted P=0.02), and 30 days after 25 mg, the SMD was -0.62 (adjusted P=.047).

The results support the researchers' parent trial, which showed an association between psilocybin therapy and reduced depression, anxiety, and motor symptoms in Parkinson's patients.

"To our knowledge, this is the first report of changes in these types of markers after psychedelic treatment in people with a neurodegenerative disease," Bradley told MedPage Today. "That gives us and other researchers super-interesting biological questions to pursue: What could be producing these changes, are they consistent in larger groups of people, and do they have anything to do with clinical benefits people with Parkinson's might experience with psilocybin?"

This research comes as part of a series of studies examining the biological effects of psychedelics as potential therapeutics for non-psychiatric conditions, said Albert Garcia-Romeu, PhD, of the Johns Hopkins University School of Medicine in Baltimore, who wasn't involved with the study. It also comes on the heels of work showing that psilocybin appeared to block nerve damage related to chemotherapy in mice, he pointed out.

Much of the work looking at psilocybin or LSD has focused squarely on mental health conditions like depression, anxiety, or addiction, Garcia-Romeu noted. "However, this study is in patients with a neurological condition -- Parkinson's disease -- and shows evidence that psilocybin may have impacted biological markers of inflammation and mitochondrial stress," he told MedPage Today.

"These new data suggest biological effects of psychedelics could be driving potential benefits in patients and pave the way for more work to better understand how psilocybin might be a useful therapeutic both in psychiatric and non-psychiatric conditions," he added.

In their open-label trial, Bradley and colleagues studied 12 people with mild-to-moderate Parkinson's disease ages 40 to 75. Participants received 10-mg and 25-mg doses of oral synthetic psilocybin approximately 2 weeks apart.

The researchers collected plasma samples from nine participants at four time points: baseline, 1 day after each psilocybin administration, and 30 days after the 25-mg dose.

The primary outcome to assess systemic inflammation was a proinflammatory index calculated as the mean z score of interleukin (IL)-6, IL-8, tumor necrosis factor alpha, interferon gamma, and high-sensitivity C-reactive protein concentrations. Mitochondrial stress was evaluated with growth differentiation factor 15 (GDF-15) and fibroblast growth factor 21 (FGF-21) measurements.

Components of the index, including IL-6, were significantly lower 1 day after the 10-mg dose but at no other time points. IL-10 was significantly higher 1 day after the 10-mg dose but not at other times.

GDF-15 was significantly lower relative to baseline 1 day after each psilocybin administration, but not from baseline 30 days after the 25-mg dose. FGF-21 was higher 1 day after each psilocybin administration, but this finding was not significant.

This was a small study of psilocybin therapy and results must be interpreted cautiously, noted co-author Aoife O'Donovan, PhD, also of UCSF. "However, the results are highly promising and suggest that more research in this area is warranted," she told MedPage Today. "We are already following this study up with more in-depth analyses of the effects of psilocybin therapy on inflammation and mitochondrial stress in a randomized controlled trial in patients with Parkinson's disease."

Work from Garcia-Romeu's lab also is studying psilocybin in a trial of people with mild cognitive impairment or early-stage Alzheimer's disease and depression. "To date, we've treated 18 individuals in that study, and enrolled 19 of a targeted 20 patients," he said. "We plan to complete the trial and publish our findings next year."