Study offers insight into how long-term inflammation may contribute to cognitive decline

Is your competent? doctor testing for this AND HAS EXACT PROTOCOLS TO STOP THE INFLAMMATION? NO? So, escaping responsibility and just blaming the stroke for your cognitive decline! I'd suggest screaming and talking to the president to get this person fired! 

 Study offers insight into how long-term inflammation may contribute to cognitive decline

The King's College London study, published in Nature Communications, offers insight into how long-term inflammation may contribute to cognitive decline in disorders such as Alzheimer's disease, aging, depression, and the lingering neurological effects of viral infections.

The scientists discovered that adding a molecule, that is involved in the inflammatory response, to stem cells from the hippocampus prevents the development of new neurons. The formation of new neurons in this region, known as hippocampal neurogenesis, is essential for learning, memory and mood regulation. It is one of the few parts of the human brain where new neurons are made in adults. Altered adult hippocampal neurogenesis is associated with aging, neurodegeneration, and mood disorders such as depression.

The study focused on cytokines, which are chemical signals that are released by the body in response to a threat, such as a viral infection. Cytokines ultimately act as triggers for the rest of the immune response, which helps the body fight the infection. High cytokine levels are also a hallmark of chronic inflammation.

Viral infection has previously been linked to changes in the ability to create new neurons in part of the hippocampus. However, how exactly infection and inflammatory cytokines affect creation of new neurons was previously unknown.

When researchers added one particular cytokine, called TNF‑α, to human hippocampal stem cells, it prevented them from developing into neurons. Instead, they switched into an "immune alert" state, releasing signals that can attract key immune cells, known as T cells, that drive inflammation, while simultaneously reducing the production of new nerve cells.

First author Dr Tinne A. D. Nissen, who completed the research as part of her PhD at King's College London, said: "What surprised us most was that the stem cells were not simply impaired by inflammation, they actively adopted behaviors that could potentially sustain immune responses in the brain."

Our findings reveal a new link between chronic inflammation and the brain's reduced ability to generate new neurons.

Inflammatory signals can effectively redirect hippocampal stem cells away from their normal role of producing neurons and toward supporting immune activity instead."

Professor Sandrine Thuret, co-corresponding author, Professor of Neuroscience, King's College London

The researchers also identified an unexpected signalling pathway behind this effect involving type I interferons, molecules typically associated with the body's antiviral defense. By blocking interferon signalling with an existing therapeutic antibody, some of the effects of inflammation were reversed – by restoring production of new neurons and preventing the attraction of T cells involved in the immune response.

Co-corresponding author Professor Linda S. Klavinskis, Professor of Viral Immunology, King's College London, added: "Our work uncovers a new mechanism that may help explain why ongoing inflammation is so damaging to brain health. Importantly, it also points to possible treatments to protect or restore the brain's regenerative capacity."

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This research was a collaboration between the Department of Infectious Diseases at the Faculty of Life Sciences & Medicine and the Department of Basic and Clinical Neuroscience at the Institute of Psychiatry, Psychology & Neuroscience, King's College London.

This research was funded by the Wellcome Trust as part of the "Neuro-Immune Interactions in Health & Disease Wellcome Trust PhD Programme, the Medical Research Council UK, a Medical Research Council Discovery Award, a PhD Studentship awarded by the Medical Research Council UK, The Galen and Hilary Weston Foundation, the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London.

Source:

King's College London

Journal reference:

Nissen, T. A. D., et al. (2026) TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells. Nature Communications. DOI: 10.1038/s41467-026-74104-x. https://www.nature.com/articles/s41467-026-74104-x

Post-stroke hippocampal neurogenesis is impaired by microvascular dysfunction and PI3K signaling in cerebral amyloid angiopathy

 What is your competent? doctor doing to get this tested and solved for in humans? Nothing? Like Usual? So you don't have a functioning stroke doctor, do you? 

Post-stroke hippocampal neurogenesis is impaired by microvascular dysfunction and PI3K signaling in cerebral amyloid angiopathy

Olivia M. Osborne¹ omo17@miami.edu ∙ Manav Daftari¹ ∙ Oandy Naranjo¹ ∙ … ∙ Anthony J. Griswold^9,10 ∙ Derek M. Dykxhoorn^9,10 ∙ Michal Toborek^1,11 mtoborek@med.miami.edu … Show more

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Highlights

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Function and tissue recovery after ischemic stroke are significantly impaired in 5xFAD mice

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Changes in the BBB reduce blood flow and reperfusion capability in the 5xFAD genotype

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Transcriptomic analysis links endothelial cells and hippocampal NPCs via the PI3K pathway

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Activation of the PI3K pathway rescues neurogenesis in 5xFAD mice post stroke

Summary

Ischemic stroke and cerebral amyloid angiopathy (CAA) pose significant challenges in an aging population, particularly in post-stroke recovery. Using the 5xFAD mouse model, we explore the relationship between CAA, ischemic stroke, and tissue recovery. We hypothesize that amyloid-beta accumulation worsens stroke outcomes by inducing blood-brain barrier (BBB) dysfunction, leading to impaired neurogenesis. Our findings show that CAA exacerbates stroke outcomes, with mice exhibiting constricted BBB microvessels, reduced cerebral blood flow, and impaired tissue recovery. Transcriptional analysis shows that endothelial cells and neural progenitor cells (NPCs) in the hippocampus exhibit differential gene expression in response to CAA and stroke, specifically targeting the phosphatidylinositol 3-kinase (PI3K) pathway. In vitro experiments with human NPCs validate these findings, showing that disruption of the CXCL12-PIK3C2A-CREB3L2 axis impairs neurogenesis. Notably, PI3K pathway activation restores neurogenesis, highlighting a potential therapeutic approach. These results suggest that CAA combined with stroke induces microvascular dysfunction and aberrant neurogenesis through this specific pathway.

Graphical abstract

The Scent of Neurogenesis: Refurbish Your Brain the Pleasurable Way

Sounds promising. But will your competent? doctor do ANYTHING AT ALL with it?

 The Scent of Neurogenesis: Refurbish Your Brain the Pleasurable Way

Sharadendu Bali*
Professor General Surgery, TMMC, TMU, Moradabad, UP, India
*Corresponding Author: Sharadendu Bali, Professor General Surgery, TMMC, TMU,
Moradabad, UP, India.
Review Article
Received: March 25, 2024
Published: April 04, 2024
© All rights are reserved by Sharadendu Bali.
1. Abstract
Neurogenesis in adult mammals is prominently observed in two specific brain regions: the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampal dentate gyrus. Neurons born in the SVZ migrate through the rostral migratory stream (RMS) to the olfactory bulb (OB), where they differentiate into interneurons. This migration is important for the sustenance and functional adaptation of the olfactory system, which is unique in its constant turnover of sensory receptor cells. The olfactory system, by its very design, maintains a direct link with the areas of the brain responsible for controlling various behaviors and emotional responses, making it a key component in the sensory-behavioral paradigm influencing adult neurogenesis. This discussion explores the mechanisms through which odors may influence the regeneration and migration of neuronal stem cells to the olfactory bulb (OB) and, consequently, affect neurogenesis.

Pot Smoking Baby Boomers Are On The Rise, Why Are Scientists So Happy For Them? Hint: Benefits For The Aging Brain

What is your doctor doing with this information? Luckily I live in a legal marijuana state and I'm not waiting for a doctor. Don't listen to me, I'm not medically trained. Is your doctor up-to-date on all research that might get you recovered?

Studies that showed improved memory, decreased brain inflammation and increased hippocampal neurogenesis in older brains after the daily stimulation of cannabinoid receptors.

Pot Smoking Baby Boomers Are On The Rise, Why Are Scientists So Happy For Them? Hint: Benefits For The Aging Brain

As cannabis users get older and/or as weed consumption among seniors becomes more common (it has quadrupled in the past seven years!) a group of scientists honed in on this large demographic of pot-smoking baby boomers..and guess what? Their results suggest that the use of whole-plant cannabis does not have a negative impact on cognition. In fact, the opposite is true.

The study, done at the University of Colorado Boulder, examined the effects of cannabis use in adults aged 60 to 88 with no history of alcohol or other substance use disorder.

Gary Wenk Ph.D., a scientist not involved in the study, noted that while high THC levels can have negative effects on the adolescent brain, quite the opposite is true with older brains. Older cannabis users, relative to non-users, have significantly greater neuronal communication between the cerebellum and hippocampus.

Why? Age-related changes in the endocannabinoid system (ECS) include a decrease in the number of cannabinoid receptors throughout the brain. The ECS, a significant aspect of our human physiology that helps maintain homeostasis, is a complex cell-signaling system in the brain and body that interacts with just about all of our other body systems.

Decreased Number Of Cannabinoid Receptors Need Stimulation, Which Means...?

During normal aging, the decline in cannabinoid receptors correlates with increased levels of inflammation in these brain regions causing a loss of neurons in the hippocampus, which is critical for learning and memory. This, in short, explains age-related memory impairment.

Very Clever Of Nature

Wenk referred to his own laboratory studies that showed improved memory, decreased brain inflammation and increased hippocampal neurogenesis in older brains after the daily stimulation of cannabinoid receptors. “The potential benefits are important given that the cerebellum and hippocampus are highly vulnerable to the effects of aging. The hippocampus is stable until around age 50, at which point the hippocampus undergoes a rapid period of atrophy,” he wrote in Psychology Today, adding that hippocampus atrophy is consistent with mild cognitive impairment. 

“The few human studies of the effect of cannabis on the brain in middle-aged or older adults found little or no negative effects on cognitive function. Longitudinal studies that compared pre- and post-exposure performance reported that cannabis was associated with improved cognitive task performance in middle-aged adults,” Dr. Wenk wrote.

"Low-dose, daily cannabis use after age 55 might effectively reduce the degenerative effects of chronic brain inflammation," Wenk concluded.

 

Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging

Lots more work to get done here.  Human testing needed. WHOM will be doing that? What is the delivery system needed for selenium? What is the amount per bodyweight and sex? 

Of course nothing was done with this earlier selenium research. Firing is needed for such cesspools of incompetence.

• selenium (3 posts to May 2015)

Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging

Author links open overlay panelOdetteLeiter¹²³⁸ZhanZhuo¹⁴⁸RuslanRust²³¹⁰Joanna M.Wasielewska²³LisaGrönnert²³¹¹SusannKowal²³Rupert W.Overall²³Vijay S.Adusumilli²³Daniel G.Blackmore¹AdamSouthon⁵KatherineGanio⁶Christopher A.McDevitt⁶NicoleRund²³DavidBrici¹Imesh AththanayakeMudiyan¹Alexander M.Sykes⁷Annette E.Rünker²³SaraZocher²³…Tara L.Walker¹²³⁹¹²

https://doi.org/10.1016/j.cmet.2022.01.005Get rights and content

Under a Creative Commons license

Open access

Highlights

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Selenium mediates the exercise-induced increase in adult hippocampal neurogenesis

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Selenium increases hippocampal precursor proliferation and adult neurogenesis

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Selenium reverses cognitive decline in aging and in hippocampal injury

Summary

Although the neurogenesis-enhancing effects of exercise have been extensively studied, the molecular mechanisms underlying this response remain unclear. Here, we propose that this is mediated by the exercise-induced systemic release of the antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, we confirmed that SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for the exercise-induced increase in adult hippocampal neurogenesis. In vivo selenium infusion increased hippocampal neural precursor cell (NPC) proliferation and adult neurogenesis. Mimicking the effect of exercise through dietary selenium supplementation restored neurogenesis and reversed the cognitive decline associated with aging and hippocampal injury, suggesting potential therapeutic relevance. These results provide a molecular mechanism linking exercise-induced changes in the systemic environment to the activation of quiescent hippocampal NPCs and their subsequent recruitment into the neurogenic trajectory.

Graphical abstract

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Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia

 

You'll have to ask your doctor if anything was done with the earlier ones or if any followup is being done with the latest. 

Effect of acute extremely low frequency electromagnetic field exposure on the antioxidant status and lipid levels in rat brain April 2012

The potential of transcranial magnetotherapy in color and rhythm therapy in the rehabilitation of ischemic stroke October 2010 

The latest here:

Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia

Qiang Gao¹ , Aaron Leung PhD ², Yong-Hong Yang³, Benson Wui-Man Lau⁴, Qian Wang⁵, Ling-Yi Liao⁶, Yun-Juan Xie⁶, Cheng-Qi He^5
1 Department of Rehabilitation Medicine, West China Hospital of Sichuan University; Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province; Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China
² Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province; Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China
³ Department of Rehabilitation Medicine, West China Hospital of Sichuan University; Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province; Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China
⁴ Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China
⁵ Department of Rehabilitation Medicine, West China Hospital of Sichuan University; Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province, China
⁶ Department of Rehabilitation Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan Province, China

Date of Submission	25-Nov-2019
Date of Decision	25-Nov-2019
Date of Acceptance	25-Aug-2020
Date of Web Publication	12-Dec-2020

Correspondence Address:
Aaron Leung
Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province; Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region
China
Cheng-Qi He
Department of Rehabilitation Medicine, West China Hospital of Sichuan University; Institute of Disaster Management and Reconstruction, Sichuan University–The Hong Kong Polytechnic University, Chengdu, Sichuan Province
China
Source of Support: This work was supported by the National Natural Science Foundation of China, No. 81201513 (to QG), Conflict of Interest: None

DOI: 10.4103/1673-5374.301020

Abstract

Extremely low frequency electromagnetic fields (ELF-EMF) can improve the learning and memory impairment of rats with Alzheimer’s disease, however, its effect on cerebral ischemia remains poorly understood. In this study, we established rat models of middle cerebral artery occlusion/reperfusion. One day after modeling, a group of rats were treated with ELF-EMF (50 Hz, 1 mT) for 2 hours daily on 28 successive days. Our results showed that rats treated with ELF-EMF required shorter swimming distances and latencies in the Morris water maze test than those of untreated rats. The number of times the platform was crossed and the time spent in the target quadrant were greater than those of untreated rats. The number of BrdU⁺/NeuN⁺ cells, representing newly born neurons, in the hippocampal subgranular zone increased more in the treated than in untreated rats. Up-regulation in the expressions of Notch1, Hes1, and Hes5 proteins, which are the key factors of the Notch signaling pathway, was greatest in the treated rats. These findings suggest that ELF-EMF can enhance hippocampal neurogenesis of rats with cerebral ischemia, possibly by affecting the Notch signaling pathway. The study was approved by the Institutional Ethics Committee of Sichuan University, China (approval No. 2019255A) on March 5, 2019.

Keywords: cerebral ischemia; cognitive function; electromagnetic fields; hippocampus; neurogenesis; plasticity; repair; signaling pathway; stroke; rat

How to cite this article: Gao Q, Leung A, Yang YH, Lau BW, Wang Q, Liao LY, Xie YJ, He CQ. Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia. Neural Regen Res 2021;16:1252-7