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Category: neuroscience – Page 3

Abstract: Implications for protecting against cognitive impairment following HeadInjury👇

Here, Michael T. Heneka & team find the inflammasome adaptor ASC drives long-lasting brain inflammation and cognitive problems after mild head injury in a closed-head injury model.

The figure shows skeletonized activated microglia (Iba1+ cells) following closed head injury, with mice lacking ASC show showing preservation of morphological features, particularly at later time points.

3Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg.

4German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

5Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.

Abstract: Immune signaling and function in neurodegeneration:

Yvonne L. Latour & Dorian B. McGavern contribute a Review to the JCI Series on Neurodegeneration, discussing signaling pathways, cellular players, and immune responses shared across multiple neurodegenerative diseases, while considering external factors that may influence CNS disease progression. Neurodegeneration.

Viral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.

Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus

Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older.

Until now.

A landmark study from researchers at the Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

Led by Dr. Ashok Shetty, university distinguished professor and associate director of the Institute for Regenerative Medicine, along with senior research scientists Dr. Madhu Leelavathi Narayana and Dr. Maheedhar Kodali, the team developed a nasal spray that, with just two doses, dramatically reduced brain inflammation, restored the brain’s cellular power plants and significantly improved memory.

The most surprising part? It all happened within weeks and lasted for months.

The findings, published in the Journal of Extracellular Vesicles, could reshape the future of neurodegenerative therapies and may even change how scientists think about brain aging itself.

Continue reading “Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus” | >

Scientists Just Took A Major Step Towards One Of Sci-Fi’s Biggest Tropes

Major milestone in the viability of cryonic suspension in the form of revival of cells after vitrification. Vitrification is basically the use of chemical fixation at ultra cold temperatures, kinda like antifreeze. It prevents ice crystals forming in your cells, preventing them from being torn apart.

It’s INSANELY toxic, so solving that problem would mean we can really revive people in suspension who underwent vitrification (which is standard practice at ALCOR for a long time now).

That said, we still will need ways to repair whatever disease or injury that the patient actually died from. 😁👍

Researchers in Germany have developed a technique to vitrify mouse brain tissue and then thaw it out, all without significant loss of function.

By cutting selected synapses, brain circuit ‘editing’ could make memory stronger and rewire how learning works

Every thought, memory, and feeling we experience depends on trillions of tiny connection points in the brain called synapses. These are the junctions where one neuron passes signals to another, forming the vast communication network known as the connectome—the brain’s wiring diagram. Although scientists have developed powerful tools to increase or decrease neural activity, directly redesigning the brain’s physical wiring has remained far more difficult.

A research team led by Dr. Sangkyu Lee and Director C. Justin Lee at the Center for Memory and Glioscience within the Institute for Basic Science (IBS), in collaboration with Dr. Kea Joo Lee of the Korea Brain Research Institute (KBRI), has now developed a molecular tool that makes such structural editing possible. The new platform, called SynTrogo (Synthetic Trogocytosis), enables researchers to induce astrocytes to selectively remodel synaptic connections in a targeted brain circuit. The paper is published in the journal Nature Communications.

The brain already has a natural mechanism for refining its wiring. During development and throughout life, unneeded or weak connections are removed in a process known as synaptic pruning, much like trimming unnecessary branches from a tree. This pruning is partly carried out by astrocytes—star-shaped glial cells that closely surround synapses and help maintain the neural environment. When this process becomes dysregulated, either through too much or too little pruning, it has been linked to disorders such as schizophrenia, autism spectrum disorder, and Alzheimer’s disease.

CRISPR Technology: Transforming the Future of Medicine and Diagnostics

Among the many promising possibilities of using CRISPR-based therapeutics, their translational use in monogenic human genetic diseases has the potential to provide long-term therapy after a single treatment. Genetic disorders can be treated with the help of CRISPR by editing the defective (disease-causing) gene or by editing the enhancer or regulator of the defective gene. Numerous studies, which are summarized in the table below (Table ), have shown promising results by using these two approaches.

3. Examples of CRISPR-Based Therapeuticsfor the Treatment of Genetic Disorders.

DiseaseCRISPR targetapproachmajor outcome of the studyreferenceDuchenne muscular dystrophydystrophin gene (DMD)single or multiplexed sgRNAs were developedto restore thedystrophin reading frame by targeting the mutational hotspot at exons45–55 and introducing shifts within exons or deleting one ormore exonsdystrophin expression is restored in vitroOusterout et al. Huntington’sdiseaseHuntingtin gene (HTT)HTT 5â€Č UTR was targetedimpropermaturation of the transcript and reducing the expressionof the disease-causing alleleKolli et al.a dual sgRNA approachwas used in vitro toexcise a 44kb promoter region upstream of a mutant HTT gene to silence its expressionexpression of the Huntington’sdisease-causing variant wasablatedShin et al.glaucomamyocilin gene (MYOC)Knocked down the expression of mutant MYOC in a mouse model of primary open-angle glaucomareductionof ER stress, lower intraocular pressure, and thepreventability of further glaucomatous damage in mouse eyes was observed. The authors also demonstrated the feasibility of utilizing CRISPR/Cas9in human eyes with glaucomaJain et al.hereditary tyrosinemiatype Ifumarylacetoacetate hydrolase gene (FAH)HDR-mediated point mutation correction in mouse hepatocytes.a significant proportion of alleles were correctedVanLith et al. Leber congenital amaurosis type 10 (LCA10)centrosomalprotein 290 gene (CEP290)AAV5-basedtherapy (EDIT-101) encapsulates Staphylococcusaureus Cas9 (SaCas9) and two sgRNAs targeting genomic locationsupstream and downstream of the intronic CEP290 pointmutation. The two sgRNAs enable cutting around the mutation to induceits removal or inversionnormal splicing of CEP290 pre-mRNA was restoredMaeder et al. Noonan syndromeleucine zipper like post translational regulator 1 gene (LZTR1)intron 16 of LZTR1 was targetedthe gene editing process could overcomethe disease phenotypeassociated with Noonan syndrome-associated cardiomyopathy in iPSC-derivedcardiomyocytes in vitroHanses et al. Angelman syndromeUBE3A-ATS Inc. RNAUBE3A-ATS Inc. RNA was targetedin cultured human neurons andin a mouse model of the diseasetargeting of UBE3A-ATSablated its function, leading to expressionof the paternal UBE3A gene and rescuing the diseasephenotypeWolter et al.congenital muscular dystrophy type 1A (MDC1A)laminin subunit alpha 1 gene (LAMA1)CRISPR activator mediated gene upregulation3.6-foldupregulation of LAMA1 was observedKemaladevi et al.genetic deafnesstransmembrane channel like 1gene (TMC1)non-homologous end joining(NHEJ)-mediated mutant Tmc alleledisruptiondeafness was prevented in mouse models upto one year postinjectionGyörgy et al.

Neuroscientist Speaks Out On The Hidden War On Consciousness

Physicist and neuroscientist Dr. Alex GĂłmez-MarĂ­n delivered a strikingly activist speech at the Science of Consciousness Conference (TSC) in Barcelona. He argued that we are now in a war on consciousness, with materialism and transhumanism forming a dangerous cocktail.

Dr. Alex GĂłmez-MarĂ­n is associate professor of the Spanish Research Council in Alicante, Spain, and director of the Pari Center in Tuscany, Italy. Hans Busstra sat down with MarĂ­n directly after his speech to analyze what this war is really about.

Our previous conversation with Marín: ‱ Blind Man Sees: Consciousness Beyond The S


You can learn more about Marín’s work at:

Our Team


https://scholar.google.com/citations?


Watch Dr. Gomez Marin’s full presentation at the Science of Consciousness Conference (TSC2025):
‱ 2025 TSC — Barcelona — Plenary 12 — End of

Other TSC interesting TSC videos: / @thescienceofconsciousness.

The Essentia Foundation wants to thank The Science Of Consciousness Conference and Robert Neville for their great support in producing this interview.

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