Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

What this blog is for:

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

Showing posts with label neuroplasticity. Show all posts
Showing posts with label neuroplasticity. Show all posts

Saturday, October 10, 2026

The limits of neuroplasticity - or are there any?

Right now, neuroplasticity is not repeatable on demand. 

When your incompetent? doctor uses this word ask then 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!

 The limits of neuroplasticity - or are there any?

Katerina Poprelka1  · Maria Stefanatou1 · Stylianos Gatzonis1 Received: 9 May 2026 / Accepted: 26 September 2026 © Fondazione Società Italiana di Neurologia 2026 

To the Editor, Cases demonstrating discordance between marked structural brain abnormalities and preserved clinical function are rare but informative. We report such a case in a 52-year old woman, highlighting the limits and resilience of neuro plastic adaptation. The patient presented to the outpatient neurology clinic following two witnessed generalized tonic-clonic seizures, both associated with a postictal phase of impaired awareness, drowsiness, and confusion, with gradual recovery over several minutes. On examination, she was alert and oriented, with no focal neurological deficits. However, deep tendon reflexes were brisk throughout, and plantar responses were indifferent bilaterally. Her past medical history was notable for childhood men ingitis, the exact etiology of which was not documented, and longstanding macrocephaly. No prior neurosurgical intervention has been reported. Despite these early neuro logical factors, she achieved normal developmental mile stones, completed secondary education, and maintained consistent employment, indicating a high level of functional adaptation. She had no history of epilepsy until the age of 43, when she began experiencing focal seizures characterized by impaired awareness, automatisms, and behavioral arrest, consistent with focal impaired awareness seizures. These were managed with lacosamide at a dose of 150 mg twice daily. In 2023, she experienced an episode of status epilepticus, precipitated by poor medication adherence. Fol lowing this, brivaracetam was added to her treatment regi men, resulting in improved seizure control. Neuroimaging revealed striking abnormalities. A CT scan demonstrated marked enlargement of the lateral and third ventricles, consistent with severe ventriculomegaly, along with significant thinning of the cortical mantle. Brain 1 Katerina Poprelka katerinapop@med.uoa.gr First Department of Neurosurgery, Evangelismos Hospital, National & Kapodistrian University of Athens, 45-47 Ipsilantou Str., Athens 10676, Greece MRI (Fig. 1) provided further detail, showing diffuse cere bral atrophy, most prominently involving the corpus cal losum, which appeared significantly thinned. Additionally, an empty sella turcica was noted. Electroencephalogra phy showed generalized slowing with predominant theta activity, intermittent epileptiform discharges, and bilateral temporo-occipital slowing, more prominent over the left hemisphere. We believe that the observed ventricular enlargement most likely reflects a long-standing developmental or post inflammatory process, rather than active hydrocephalus. The available clinical and imaging data do not allow a clear distinction between chronic post-infectious hydrocephalus, arrested hydrocephalus, and long-standing overt ventriculo megaly in adults (LOVA). The degree of ventricular enlarge ment is disproportionate to the observed cortical atrophy, making hydrocephalus ex vacuo less likely. We therefore favor a multifactorial explanation involving chronic ventric ulomegaly with secondary cerebral atrophy, while acknowl edging the inherent diagnostic uncertainty. A comprehensive neuropsychological assessment was conducted to evaluate cognitive functions in greater depth. Mild executive dysfunction was observed, particularly affecting cognitive flexibility, planning, and processing speed, as evidenced by reduced performance on Stroop Neuropsychological Screening Test, Trail Making Test Part B, and Digit Symbol Coding. Memory performance was dis proportionately affected, with severe impairments in verbal and visual learning and delayed recall on the Rey Auditory Verbal Learning Test and the Rey-Osterrieth Complex Fig ure Test, suggesting deficits across encoding, consolidation, and retrieval processes. Increased susceptibility to interfer ence was also observed. The non-modality-specific pattern, affecting both verbal and visual memory, points to dysfunc tion within distributed memory networks rather than a focal deficit. Despite these objective deficits, the patient did not report significant subjective cognitive complaints in daily life. However, cognitive fatigue was observed during test ing, which may have contributed to reduced performance and suggests limited cognitive reserve under sustained  demand. Importantly, there was no evidence of coexisting mood or anxiety disorders that could otherwise explain or exacerbate cognitive findings. The prevalence of hydrocephalus in the adult population is estimated at roughly 1 per 10,000, with aqueductal steno sis accounting for approximately 10% of cases [1]. Additional common etiologies include congenital abnormalities, infec tious processes, head trauma, and space-occupying obstructive lesions. Among these etiologies, long-standing hydrocepha lus, including cases secondary to early-life insults such as infection, is of particular interest, as it may be associated with severe anatomical distortion yet relatively preserved clini cal function. This case demonstrates a marked dissociation between extensive structural brain abnormalities and func tional outcome. Although the degree of ventriculomegaly, cor tical thinning, and diffuse atrophy would typically be expected to result in significant neurological and cognitive impairment, the most striking feature in this patient is the preservation of functional independence despite objectively significant neu ropsychological deficits, including severe memory impair ment and mild executive dysfunction. Notwithstanding these findings, she maintained autonomy in everyday activities for decades, underscoring a complex and non-linear relationship between cognitive impairment and real-world functioning. Similar cases have been described in the literature, particularly in individuals with long-standing or congenital hydrocepha lus, in whom profound anatomical distortion is accompanied by relatively mild clinical manifestations [2, 3]. A 44-year-old man with a history of childhood hydro cephalus and shunt placement demonstrated severe ventricu lomegaly and a markedly thin cortical mantle, accompanied by low-average intellectual functioning; nevertheless, he maintained functional independence and relatively stable neurological status over time, with cognitive deficits that appeared chronic rather than progressive [2]. Similarly, in a (C) Sagittal and coronal views illustrating the marked expansion of the ventricular system and compression of the brain parenchyma 72-year-old woman with overt ventriculomegaly, preserved independence and normal cognitive screening were reported despite severe structural abnormalities, with seizures emerg ing late in life in the context of otherwise minimal neurolog ical impairment [3]. Compared with these cases, the present patient shares the characteristic dissociation between severe structural brain changes and preserved daily functioning; however, she is distinguished by more pronounced memory impairment on formal neuropsychological testing despite long-term independence. These observations may be considered within the frame work of developmental plasticity, whereby cognitive func tions developing in the context of early neurodevelopmental abnormalities may adapt to an atypical neural substrate. In this context, adaptation is more appropriately conceptual ized as the development of cognitive functions within exist ing structural constraints rather than as “reorganization” of previously established networks. Such developmental adaptation may partly account for the preservation of func tional independence despite severe structural abnormalities, although the mechanisms underlying this dissociation can not be established from the present case. The presence of significant memory impairment and milder executive dys function, together with the later emergence of epilepsy, nev ertheless suggests that this adaptation may be incomplete and may not fully protect against cognitive and neurological vulnerability. Cognitive reserve may also have contributed to the relatively preserved everyday functioning; however, available proxies are limited to educational attainment and sustained employment, precluding stronger conclusions regarding its role. Age-related changes, increasing network inefficiency, and reduced cognitive reserve have been pro posed as factors that may reveal previously compensated vulnerabilities over time; however, their contribution in the present case remains speculative 
In summary, this case highlights that functional outcome in chronic structural brain disease is not determined solely by anatomical integrity. Instead, the marked dissociation between structural abnormalities and everyday functioning may reflect the influence of developmental adaptation and individual differences in cognitive reserve, although their respective contributions cannot be established in this case. While the brain demonstrates remarkable adaptability in the context of longstanding structural abnormalities, cognitive deficits and neurological complications may still emerge, underscoring the importance of comprehensive evaluation and long-term follow-up. 
Author Contribution Credit authorship contribution statement Kateri na Poprelka: Conceptualization, Investigation, Formal Analysis, Writ ing Original Draft. Maria Stefanatou: Validation, Writing- Review & Editing. Stylianos Gatzonis: Supervision, Writing- Review & Editing. Funding No funding was received to assist with the preparation of this manuscript. Declarations Ethics approval The authors have obtained patient consent. Competing interest The authors have no competing interests to de clare that are relevant to the content of this article. References 1. 2. 3. Oi S, Shimoda M, Shibata M, Honda Y, Togo K, Shinoda M, Tsu gane R, Sato O (2000) Pathophysiology of long-standing overt ventriculomegaly in adults. J Neurosurg 92:933–940. h t t p s : / / d o i . o r g / 1 0 . 3 1 7 1 / j n s . 2 0 0 0 . 9 2 . 6 . 0 9 3 3 Feuillet L, Dufour H, Pelletier J (2007) Brain of a white-collar worker. Lancet 370:262. h t t p s : / / d o i . o r g / 1 0 . 1 0 1 6 / S 0 1 4 0 - 6 7 3 6 ( 0 7 ) 6 1 1 2 7 - 1 Persad AR, Bass V, Meguro K (2021) Asymptomatic hydrocepha lus. CMAJ 193:E480. https: //d oi. or g/10 .150 3/cmaj.200889 Publisher’s Note Springer Nature remains neutral with regard to juris dictional claims in published maps and institutional affiliations

Monday, September 28, 2026

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.

This shows a brain.
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

Monday, July 27, 2026

Wednesday, July 15, 2026

Can doing nothing create neuroplasticity?

 Yes, doing nothing actively fuels neuroplasticity. When your brain is idle, it activates the Default Mode Network (DMN). 

ASK YOUR COMPETENT? DOCTOR EXACTLY HOW MUCH OF DOING NOTHING WILL GET YOU RECOVERED!

This is covered in the book; 'The Brain at Rest; How the Art and Science of Doing Nothing can Improve Your Life'

And 'Niksen: Embracing the Dutch Art of Doing Nothing'!

Monday, June 29, 2026

The effect of probiotic supplements on cognitive outcomes and neuroplasticity in elderly ischemic stroke survivors

 How soon will your competent? doctor and dietician update your diet protocols? Oh NO, you don't have any, do you?

The effect of probiotic supplements on cognitive outcomes and neuroplasticity in elderly ischemic stroke survivors


  • 1. Department of Neurology, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

  • 2. Department of General Affairs, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

Abstract

Background: 

This retrospective cohort study investigates the effects of probiotic supplementation on the nutritional, cognitive, and motor functions of elderly survivors recovering from ischemic stroke. Given the high prevalence of nutritional deficits and cognitive impairments in this population, exploring adjunct therapies such as probiotics could provide improved outcomes.

Methods: 

The study included 223 elderly ischemic stroke survivors treated between March 2021 and February 2024, divided into two groups based on treatment modalities: the Conventional Group (n = 117) receiving standard enteral nutrition, and the Supplement Group (n = 106) receiving similar nutrition plus probiotics. Data collected included NIH Stroke Scale (NIHSS), nutritional indicators, cognitive assessments (MMSE, HDS, CDR, SES), and motor evaluations (STREAM, mRS, MBI).

Results: 

Baseline comparisons showed no significant differences between groups. Post-treatment outcomes demonstrated significant improvements in the Supplement Group across several measures. Neurotrophic and nutritional parameters, including BDNF, hemoglobin, albumin, and prealbumin levels, significantly increased (p ≤ 0.011). Cognitive function also improved, with higher MMSE and HDS scores and reduced CDR scores (p < 0.003). Motor function, evaluated by STREAM, showed enhanced upper and lower limb mobility and basic activities (p ≤ 0.014). Further, participants in the Supplement Group experienced better functional recovery with decreased mRS scores and increased MBI scores (p < 0.004). The incidence of gastrointestinal adverse events was significantly reduced in the Supplement Group (p < 0.001), and correlation analysis underscored positive associations between probiotics and improved outcomes (p ≤ 0.003).

Conclusion: 

Probiotic supplementation as part of nutritional therapy significantly enhances nutritional, cognitive, and motor function recovery in elderly ischemic stroke survivors, while also reducing gastrointestinal adverse events. These findings suggest that incorporating probiotics into recovery protocols post-stroke may facilitate better health outcomes and provide a well-tolerated therapeutic adjunct.


More at link.

Monday, May 11, 2026

Mechanisms of Action and Advances in Application of Music Therapy in Improving Cognitive Impairment Based on the Theory of Neuroplasticity

 We know music therapy works in stroke; but does your incompetent? doctor even have a protocol for you?

Mechanisms of Action and Advances in Application of Music Therapy in Improving Cognitive Impairment Based on the Theory of Neuroplasticity


  • Hunan University of Chinese Medicine, Changsha, China

The final, formatted version of the article will be published soon.

    Abstract

    As global population aging accelerates, preventing and treating cognitive impairment has become a major public health priority. Music therapy is a safe, well-tolerated non-pharmacological intervention with substantial potential to improve cognitive function. This review synthesizes the neurologic music therapy (NMT) framework, encompassing techniques targeting attention, memory, and executive function, delivered through both active and receptive approaches. Clinical investigations indicate that music therapy may improve cognition and neuropsychiatric symptoms in Alzheimer's disease (AD), vascular cognitive impairment (VCI), Parkinson's disease–related cognitive impairment, mild cognitive impairment (MCI), and traumatic brain injury (TBI); however, effects appear to vary by intervention duration and disease stage. This narrative review aims to provide a theoretical foundation and practical guidance for the non-pharmacological intervention of cognitive impairment by collating evidence on the neuroplasticity theoretical foundations, technical systems, and clinical applications of music therapy.

    Summary


    Copyright

    © 2026 Zeng, Tang, Wang, Lei, Xing, Wang and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    Saturday, May 9, 2026

    7 Best Brain-Boosting Superfoods to Eat for Neuroplasticity After Stroke to Optimize Recovery by Flint Rehab

     These should all be in your diet protocol if your doctor and dietician ARE ANY GOOD AT ALL! Oh sorry, not good, you have NO diet protocol, do you?

    Let's check how long incompetence has existed for each one!


    7 Best Brain-Boosting Superfoods to Eat for Neuroplasticity After Stroke to Optimize Recovery

    7 Best Brain-Boosting Foods to Eat After Stroke

    1. Blueberries

    2. Fatty Fish

    .

    3. Leafy Green Vegetables


    4. Walnuts


    5. Avocados


    6. Turmeric

    .

    7. Dark Chocolate

    Full details at link.

    Tuesday, April 21, 2026

    Yoga, AI, and Neuroplasticity: Navigating the Pathways to Cognitive Resilience

    I need as much cognitive reserve and resilience as possible since I probably used all of mine up just surviving my stroke. Ask your competent? doctor for EXACT PROTOCOLS TO BUILD RESILIENCE AND RESERVE! Your doctor NEEDS TO GUARANTEE REBUILDING YOUR RESERVE TO PREVENT DEMENTIA!

     Yoga, AI, and Neuroplasticity: Navigating the Pathways to Cognitive Resilience

    Siddhant Rajhans1*, Dr. Somlata Jha2, Prakhar Singh3, Anuj Anand4, Vaibhav Saini5 1*Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan University, India. siddhantrajhanssrhu@zohomail.in 2 Assistant Professor, School Of Yogic Science, Swami Rama Himalayan University, India 3Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan University, India. 4Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan University, India. 5 Department Of Computer Science, Vivekananda Institute Of Professional Studies, India *Corresponding Author: Siddhant Rajhans siddhantrajhanssrhu@zohomail.in 

     Abstract 

     In this ever-changing modern world, people should be highly adaptable and have the ability to adjust to any situation. We aim to do extensive research on the relationships that exist between yoga, neuroplasticity, and artificial intelligence (AI), and also the methods for developing a high level of cognitive resilience. In order to identify pathways to cognitive wellbeing, we examine the cultural foundations of yoga, the transformative potential of AI, and neuroplasticity in this paper. To get the most useful understanding of how to promote cognitive resilience, people must be able to recognise the intersection and synergy between these components. Only then will they be able to learn how to promote cognitive resilience when confronted with life's challenges, as well as how to think differently going forward by applying these useful strategies. 

    Thursday, April 16, 2026

    Naringin Reverses Chronic Stress-Induced Cognitive Deficits and Enhances Hippocampal Neuroplasticity in Mice

     

    All stroke patients are under massive stress because your incompetent? doctor doesn't have 100% RECOVERY PROTOCOLS. Will you doctor and hospital get human testing going?

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

    OH NO! your doctor KNOWS NOTHING AND DOES NOTHING! 

    Here's all the previous information on naringin which your incompetent doctor doesn't know about, have them prove me wrong!

    You do expect your doctor to be up-to-date on stroke research? Otherwise, you would be selecting a better doctor, right?

    Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice 2010 


    Preventive effects of hesperidin, glucosyl hesperidin and naringin on hypertension and cerebral thrombosis in stroke‐prone spontaneously hypertensive rats 2012


    Therapeutic potential of naringin in neurological disorders 2019


    Naringin reverses neurobehavioral and biochemical alterations in intracerebroventricular collagenase-induced intracerebral hemorrhage in rats 2017


    The beneficial role of Naringin-a citrus bioflavonoid, against oxidative stress-induced neurobehavioral disorders and cognitive dysfunction in rodents: A systematic … 2017


    Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain 2009


    Naringin attenuates cerebral ischemia-reperfusion injury through inhibiting peroxynitrite-mediated mitophagy activation 2018


    The effect of ozone and naringin on intestinal ischemia/reperfusion injury in an experimental model 2015


    Preclinical evidence for the pharmacological actions of naringin: a review 2014

    And that's just the first page of 'naringin and stroke' in Google Scholar. 

    The latest here:

    Naringin Reverses Chronic Stress-Induced Cognitive Deficits and Enhances Hippocampal Neuroplasticity in Mice


    Abstract

    Chronic stress, such as chronic unpredictable mild stress (CUMS), induces hippocampal oxidative stress, inflammation, and neurochemical imbalances, resulting in cognitive and synaptic deficits. However, the role of naringin, a citrus bioflavonoid with antioxidant and neurotrophic properties in reversing hippocampal oxidative–inflammatory effects in CUMS remains largely unexplored. This study uniquely elucidates the neurocognitive and synaptic mechanisms through which naringin restores hippocampal integrity, emphasizing its dual antioxidant and neurogenic actions against CUMS-induced cognitive dysfunction. Adult male mice were divided into six groups (n = 9/group): control, CUMS, naringin (2.5, 5, 10 mg/kg), and fluoxetine (10 mg/kg). All mice except the control group were exposed to CUMS daily for 21 days. After 21 days of treatment post-CUMS exposure, behavioral assessments, biochemical assays, immunohistochemical assay for neuroplasticity-related proteins, and histological analyses were conducted. Naringin significantly improved memory performance in the Y-Maze and NORT, as evidenced by increased % alternation and discrimination index. Naringin significantly reduced nitrite and acetylcholinesterase enzyme activity while attenuating the depletion of reduced glutathione, superoxide dismutase and catalase activities in the brains of CUMS mice. CUMS exposure increased proinflammatory cytokines (TNF-α and IL1-β), which were attenuated by naringin. Likewise, hippocampal neurotransmitters, including serotonin, dopamine and noradrenaline, were restored by naringin relative to CUMS group. Naringin upregulated neurotrophic (BDNF), neuronal (NeuN), and proliferative (Ki-67) markers while suppressing astroglia activation (GFAP), indicating enhanced neuronal survival, synaptic remodeling, and hippocampal neurogenesis that collectively supported behavioral recovery. In conclusion, naringin ameliorates CUMS-induced cognitive impairment through inhibition of oxidative stress, inflammation, neurotransmitter imbalance, and enhancing hippocampal neurogenesis.