Images of sagittal sections through the corpus callosum were acquired at 5,000× magnification for measurements of axon diameter and myelin thickness along with manual counting of degenerating axons, demyelinated axons, and excessive myelin figures. Analysis included 3 to 5 images per animal (at least 120 axons per image); 3 to 6 animals per condition were used. Degenerating axons were defined as axons with cytoskeletal changes (microtubule and neurofilament density extremely low or high with irregular spacing), axons filled with vesicles, or axons with swollen mitochondria (filling >50% of the axon cross-section). Demyelinated axons were manually counted based on a lack of detectable compact myelin and a diameter larger than 0.3 μm. Axons smaller than 0.3 μm were excluded from analysis as potentially unmyelinated fibers (27 (link)). An excessive myelin figure was identified as a myelin sheath that was not tightly enwrapping an axon but instead folded back on itself (i.e. redundant myelin) (13 (link), 22 (link)). These figures can be seen surrounding and extending from an intact axon or a degenerating axon or remaining without an axon. Within each counting frame, all apparently intact axons were measured to determine axon diameter and myelin thickness using Metamorph software (Molecular Devices), as previously detailed (28 (link), 29 (link)). These values were also used to calculate the g-ratio (axon diameter divided by myelinated fiber diameter) as an indicator of remyelination. Excessive myelin figures were measured along the lumen of the myelin sheaths, and that length was doubled to determine the length of each excessive myelin figure. Additional images were taken at 10,000× for illustration of pathology. Quantification included 26 mice (3 days: n = 3 sham, n = 4 TBI; 1 week: n = 5 TBI; 2 weeks: n = 5 TBI; 6 weeks: n = 4 sham, n = 5 TBI).
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Remyelination
Remyelination
Remyelination is the process of regenerating the myelin sheath, a protective layer that surrounds nerve fibers, after damage or loss.
This crucial process allows for the restoration of efficient nerve signal transmission, which is essential for proper neurological function.
Remyelination research explores the biological mechanisms, therapies, and strategies to promote the regrowth of myelin in conditions such as multiple sclerosis, traumatic brain injury, and other demyelinating disorders.
By understanding the complex pathways involved in remyelination, scientists can develop innovative approaches to enhance the body's natural repair capabilities and improve outcomes for patients affected by these debilitating neurological conditions.
This crucial process allows for the restoration of efficient nerve signal transmission, which is essential for proper neurological function.
Remyelination research explores the biological mechanisms, therapies, and strategies to promote the regrowth of myelin in conditions such as multiple sclerosis, traumatic brain injury, and other demyelinating disorders.
By understanding the complex pathways involved in remyelination, scientists can develop innovative approaches to enhance the body's natural repair capabilities and improve outcomes for patients affected by these debilitating neurological conditions.
Most cited protocols related to «Remyelination»
Animals
Axon
Corpus Callosum
Cytoskeleton
Fibrosis
Medical Devices
Mice, House
Microtubules
Mitochondria
Myelin Sheath
Neurofilaments
Reading Frames
Remyelination
Vision
Animals
Animals, Laboratory
Cuprizone
Demyelination
Diet
Eating
Food
Males
Mice, House
Pellets, Drug
Remyelination
Rodent
Vacuum
P1–P2 mouse pups were decapitated, and their brains or spinal cords were dissected into ice-cold Hank's Balanced Salt Solution (HBSS). 200–300 μm sagittal slices of cerebellum, brainstem or spinal cord were cut using a McIlwain tissue chopper. The slices were placed on Millipore Millicell-CM organotypic culture inserts (Fisher) in medium containing 50% MEM with Earle's salts, 25% Earle's Balanced Salt Solution, 25% heat-inactivated horse serum (HIHS), glutamax-II supplement with penicillin–streptomycin, amphotericin B (all purchased from Invitrogen) and 6.5 mg/ml glucose (Sigma). Medium was changed every two days. After 10 days in culture, demyelination was induced by addition of 0.5 mg/ml lysophosphatidylcholine (lysolecithin, LPC, Sigma) to the medium for 15–20 h, after which slices were transferred back into normal medium. Cerebellar slice cultures require around 16 h, whereas brainstem and spinal cord cultures require around 18 h of incubation. Concentrations of LPC higher than this are also toxic to axons. Medium containing factors was added 12 h later. Factors used were Platelet Derived Growth Factor (PDGF) (10 ng/ml, teproTech Inc.), Fibroblast growth factor (FGF) (10 ng/ml, teproTech Inc.), Neuregulin 1 (NRG1) (10 ng/ml, R&D Systems), NRG1-III (10 ng/ml, R&D Systems), DAPT (gamma secretase inhibitor, 5 μM, CalBiochem), 9-cis retinoic acid (9cRA, 50 nM, Sigma), 9cRA agonists HX630 and PA024, and 9cRA antagonist PA452 (1 μM, 500 nM, 5 μM respectively, kindly supplied by Hiroyuki Kagechika). Cultures were maintained for a further 14 days, and then processed for immunolabelling. For proliferation assays, BRDU (Roche) was added for 16 h to the culture medium before fixation at DIV10 (myelination M), DIV12 (demyelination DM) and DIV25 (remyelination RM).
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1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol
agonists
Alitretinoin
Amphotericin B
Axon
Biological Assay
Brain
Brain Stem
Bromodeoxyuridine
Cerebellum
Cold Temperature
Culture Media
Demyelination
Dietary Supplements
Equus caballus
gamma-Secretase
Glucose
Hanks Balanced Salt Solution
HX 630
Lysophosphatidylcholines
Microphysiological Systems
Mus
Myelin Sheath
Neuregulin 1
Penicillins
Platelet-Derived Growth Factor
Remyelination
Salts
Serum
Sodium Chloride
Spinal Cord
Streptomycin
Tissues
Acrolein
Axon
Cuprizone
Demyelination
Electron Microscopy
Fibrosis
Immunoglobulins
Immunohistochemistry
Medical Devices
Mice, House
Microscopy, Confocal
Neurofilaments
paraform
Rabbits
Remyelination
Tamoxifen
Tissues
Tongue
Transmission Electron Microscopy
Biopharmaceuticals
Brain
Cells
Cuprizone
Demyelination
Homo sapiens
Immunohistochemistry
Lysophosphatidylcholines
Mus
Myelin Sheath
Oligodendroglia
Patients
Population Group
Proteins
Remyelination
Tissues
Most recents protocols related to «Remyelination»
Sections were incubated in citrate buffer (pH=6.0) at 98°C and then cooled and rinsed for 3×5 min in TRIS tampon (pH=7.6). They were incubated in a 3% H2O2 blocked endogenous peroxidase activity for 5 min at room temperature and rinsed for 3×5 min in TRIS tampon. Blockage of nonspecific binding protein was done by incubating sections with horse serum (Sigma Aldrich, H1138) for 30 min. Incubation with anti-EphA4 primary antibody (Santa Cruz, sc-365503) was done overnight at 4°C. After rinsed for 3×5 min in TRIS tampon, the sections were incubated with donkey anti-mouse IgM secondary antibody (Jackson Immunoresearch, 715-065-140) for 1 h and ABC solution (VECTOR Laboratories, PK6100) for 2 h. The reactions were visualized with DAB and counterstained with Harris haematoxylin.
Results were independently evaluated by two investigators using a light microscope. Fibrosis, inflammation, and degeneration were evaluated on a three-point scale (mild, moderate, and severe). Regenerative changes around the nerve (remyelination and EphA4 receptor expression) were evaluated on a five-point scale (none, poorly, moderate, well, and perfect). Photographs were taken using an Olympus BX 50 photomicroscope.
Results were independently evaluated by two investigators using a light microscope. Fibrosis, inflammation, and degeneration were evaluated on a three-point scale (mild, moderate, and severe). Regenerative changes around the nerve (remyelination and EphA4 receptor expression) were evaluated on a five-point scale (none, poorly, moderate, well, and perfect). Photographs were taken using an Olympus BX 50 photomicroscope.
anti-IgM
Antibodies, Anti-Idiotypic
Binding Proteins
Buffers
Citrates
Cloning Vectors
Equus asinus
Equus caballus
Fibrosis
Hematoxylin
Immunoglobulins
Inflammation
Light Microscopy
Mus
Nerve Regeneration
Peroxidase
Peroxide, Hydrogen
Receptor, EphA4
Remyelination
Serum
Tromethamine
Animal use and drug administration were described in our previous study (Chen et al., 2021 ). GFAP-tTA mice on a C57BL/6J background were mated with TRE-IFN-γ mice on a C57BL/6J background to produce GFAP-tTA; TRE-IFN-γ double-transgenic mice. These mice were given 200 ppm Dox (Envigo, Madison, WI) from conception to prevent transcriptional activation of IFN-γ. The Dox diet was discontinued and replaced with a 0.2% cuprizone diet (Envigo, Madison, WI) starting at six weeks of age. Cuprizone feeding lasted five weeks and then the mice were placed back on normal chow for up to two weeks to allow early remyelination to occur. Concurrently, 8 mg/kg of Sephin1 (i.p.) (#SM1356, Sigma, St. Louis, MO) or 10 mg/kg of BZA (gavage) (#PZ0018, Sigma) were given daily to the GFAP-tTA; TRE-IFN-γ mice, starting from three weeks of cuprizone exposure. The corpus callosum of each mouse was collected two weeks after cuprizone feeding cessation.
EAE was induced in 9-week-old female C57BL/6J mice (Jackson Laboratories, Bar Harbor, ME) by subcutaneous flank administration of 200 µg MOG35–55 peptide emulsified with complete Freund’s adjuvant (CFA) and killed Mycobacterium tuberculosis H37Ra (#EK2100 kit, Hookes Laboratory, Lawrence, MA). Intraperitoneal (i.p.) injections of 200 ng pertussis toxin were given immediately after administration of the MOG emulsion and again 24 hours later. Mice were blindly scored daily for clinical signs of EAE from 0 (no symptoms) to 5 (most severe). Mice were put on a 2BAct diet, which was generously provided by Dr. Carmela Sidrauski’s group (Calico Life Sciences, South San Francisco, CA), two days before EAE induction. Daily treatment with i.p Sephin1 at 8mg/kg were started seven days after EAE induction. The treatment of the animals used in this study was conducted in accordance with the ARRIVE guidelines and in complete compliance with the Animal Care and Use Committee guidelines of Northwestern University.
EAE was induced in 9-week-old female C57BL/6J mice (Jackson Laboratories, Bar Harbor, ME) by subcutaneous flank administration of 200 µg MOG35–55 peptide emulsified with complete Freund’s adjuvant (CFA) and killed Mycobacterium tuberculosis H37Ra (#EK2100 kit, Hookes Laboratory, Lawrence, MA). Intraperitoneal (i.p.) injections of 200 ng pertussis toxin were given immediately after administration of the MOG emulsion and again 24 hours later. Mice were blindly scored daily for clinical signs of EAE from 0 (no symptoms) to 5 (most severe). Mice were put on a 2BAct diet, which was generously provided by Dr. Carmela Sidrauski’s group (Calico Life Sciences, South San Francisco, CA), two days before EAE induction. Daily treatment with i.p Sephin1 at 8mg/kg were started seven days after EAE induction. The treatment of the animals used in this study was conducted in accordance with the ARRIVE guidelines and in complete compliance with the Animal Care and Use Committee guidelines of Northwestern University.
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Animals
Conception
Corpus Callosum
Cuprizone
Diet
Emulsions
Freund's Adjuvant
Glial Fibrillary Acidic Protein
IFNG protein, mouse
Interferon Type II
Mice, House
Mice, Inbred C57BL
Mice, Transgenic
Mycobacterium tuberculosis
Peptides
Pertussis
Remyelination
scorpion toxin I''
sephin1
Transcriptional Activation
Tube Feeding
Woman
SSEP will be performed at baseline, and at 12 and 24 weeks to assess remyelination (Cadwell Elite, Kennewick, Washington, USA). SSEP will be recorded after median nerve and posterior nerve electrical stimulation starting with a square pulse of 0.2 ms duration at a rate of 3.11 Hz at 2 mA above motor threshold. The averages of two or more subsequent runs (at least 2×500 pulses) will be inspected for reproducibility and the mean will be used for analysis. For the upper extremities, active surface electrodes will be placed at C3’/C4’ contralateral to stimulation (reference: Fz) to obtain N20. For the lower extremities, active surface electrodes will be placed at Cz (reference: Fz) to obtain P40. Recordings will follow the recommendations of the American Clinical Neurophysiology Society.33 (link) Prolonged latencies of N20 or P40 reflect demyelination within the upper and lower extremity sensory pathways, respectively.20 SSEP latency z-scores for each limb will be calculated using previously established normative values.34 (link)
Demyelination
Lower Extremity
Nerves, Median
Nervousness
Pulse Rate
Pulses
Remyelination
Stimulations, Electric
Upper Extremity
Mobility tests will be conducted at baseline, 12 and 24 weeks. Exercise endurance will be evaluated with the 6-Minute Timed Walk (6MTW).35 (link) Participants will be asked to walk for 6 min and the total distance will be recorded. Walking mobility will be measured with the Timed Up and Go (TUG).36 (link) Participants will be asked to stand up from a chair, walk 7 metres, turn, return to the chair, turn and sit down. The average of two timed tests will be recorded. Walking speed will be measured by the Timed 25-Foot Walk (T25FW).37 (link) To estimate fall frequency, participants will be asked how many falls they have sustained in the prior 30 days. Upper extremity mobility will be measured with the 9 Hole Peg Test (9HPT).37 (link) During this test the time for participants to place nine pegs into a platform with holes and then take them out again will be measured. MS disability will be measured with the MS Functional Composite (MSFC), a three-part, standardised, quantitative, assessment instrument in MS clinical trials measuring cognition, leg function and arm/hand function and will be calculated using the T25FW, 9HPT and Symbol Digit Modalities Test (SDMT, described in Cognitive Function below).37 38 (link)
Participants will perform the 6MTW and TUG wearing wireless, synchronised inertial sensors on both wrists and ankles as well as on the torso at lumbar vertebra level 5 and chest (superior sternum level).39 (link) These inertial sensors record three-dimensional linear acceleration and angular velocities. Participants will also be asked to stand quietly with their hands on hips and their eyes open and closed for 30 s each with the sensors on to measure postural sway. These body worn sensors provide robust and quantitative measurements of multiple gait parameters that are reliable in pwMS39 (link) and are more sensitive than the T25FW for gait dysfunction in early MS.40 (link) These metrics also correlate strongly with fall frequency41 (link) and were successfully employed in our group’s previous clinical trial of lipoic acid.42 (link)
Of the aforementioned mobility outcomes (ie, 6MTW, TUG, T25FW, MSFC), the one with the strongest correlation with SSEP latency in part 1 of the study will become the primary clinical outcome to measure remyelination in part 2 of this clinical trial.
Participants will perform the 6MTW and TUG wearing wireless, synchronised inertial sensors on both wrists and ankles as well as on the torso at lumbar vertebra level 5 and chest (superior sternum level).39 (link) These inertial sensors record three-dimensional linear acceleration and angular velocities. Participants will also be asked to stand quietly with their hands on hips and their eyes open and closed for 30 s each with the sensors on to measure postural sway. These body worn sensors provide robust and quantitative measurements of multiple gait parameters that are reliable in pwMS39 (link) and are more sensitive than the T25FW for gait dysfunction in early MS.40 (link) These metrics also correlate strongly with fall frequency41 (link) and were successfully employed in our group’s previous clinical trial of lipoic acid.42 (link)
Of the aforementioned mobility outcomes (ie, 6MTW, TUG, T25FW, MSFC), the one with the strongest correlation with SSEP latency in part 1 of the study will become the primary clinical outcome to measure remyelination in part 2 of this clinical trial.
Acceleration
Ankle
Chest
Cognition
Coxa
Disabled Persons
Eye
Foot
Human Body
Range of Motion, Articular
Remyelination
Sternum
Thioctic Acid
Torso
Upper Extremity
Vertebrae, Lumbar
Wrist
The original hard copies of study data will be stored in a locked office and de-identified data will be saved on a secure electronic database. De-identified data will be added to an institutional repository after study completion. Data analysis will be overseen by a biostatistician. To determine the relationship between SSEP and measures of clinical disability and mobility, we will perform partial correlations between SSEP P40 and 6MTW, T25FW, MSFC, TUG, postural sway and other body-worn sensor measurements, fall frequency and lower extremity Neuro-QOL at baseline. We will also perform partial correlations to examine associations between SSEP N20 and upper extremity dexterity (9HPT) and upper extremity Neuro-QOL. In performing partial correlations, we will control for muscle strength, relevant demographic variables and disease factors, as needed. As an exploratory outcome, we will also perform partial correlations to examine associations between body structures (VO2max, quadricep and hamstring muscle strength, hand grip) and the mobility measures listed above. These analyses will include all participants who provide baseline data.
To determine the safety and feasibility of the cycling intervention, we will track retention and adherence. Adherence will be measured as the number of sessions completed, with successful completion defined as participation in ≥80% of MSCYCLE or MSTC sessions. For MSCYCLE participants, we will perform a subanalysis to examine correlations between average time spent in the target HR zone and improvement in SSEP outcomes and improvement in aerobic fitness as measured by VO2max.
To determine whether the cycling intervention is associated with clinical and objective evidence of remyelination, we will perform mixed effect linear regression analyses to model change in clinical measures and SSEP N20 and P40 from baseline to 12 and 24 weeks in active (n=22) and control (n=22) participants. Regression models will include random effects for participants and for limbs within participants. We will also perform a subanalysis looking at only the worst leg. Determination of the primary clinical outcome for part 2 of the study will be made after analysis of baseline data (see Mobility and Disability Outcomes, above), and will be determined before model building begins. Associations between change in SSEP latency and changes in walking-related outcomes will be analysed by linear regression or analyses of correlation (eg, Pearson’s correlation) on the change scores. To model change in MWF from baseline to 24 weeks, we will perform mixed effects linear regression analyses in active (n=11) and control (n=11) participants of the corpus callosum, bilateral internal capsules and MS lesions. For all analyses involving multiple testing, an appropriate method of controlling the family-wise error or false detection rate will be chosen prior to beginning the analyses.
To determine the safety and feasibility of the cycling intervention, we will track retention and adherence. Adherence will be measured as the number of sessions completed, with successful completion defined as participation in ≥80% of MSCYCLE or MSTC sessions. For MSCYCLE participants, we will perform a subanalysis to examine correlations between average time spent in the target HR zone and improvement in SSEP outcomes and improvement in aerobic fitness as measured by VO2max.
To determine whether the cycling intervention is associated with clinical and objective evidence of remyelination, we will perform mixed effect linear regression analyses to model change in clinical measures and SSEP N20 and P40 from baseline to 12 and 24 weeks in active (n=22) and control (n=22) participants. Regression models will include random effects for participants and for limbs within participants. We will also perform a subanalysis looking at only the worst leg. Determination of the primary clinical outcome for part 2 of the study will be made after analysis of baseline data (see Mobility and Disability Outcomes, above), and will be determined before model building begins. Associations between change in SSEP latency and changes in walking-related outcomes will be analysed by linear regression or analyses of correlation (eg, Pearson’s correlation) on the change scores. To model change in MWF from baseline to 24 weeks, we will perform mixed effects linear regression analyses in active (n=11) and control (n=11) participants of the corpus callosum, bilateral internal capsules and MS lesions. For all analyses involving multiple testing, an appropriate method of controlling the family-wise error or false detection rate will be chosen prior to beginning the analyses.
Corpus Callosum
Disabled Persons
Exercise, Aerobic
Grasp
Human Body
Internal Capsule
Lower Extremity
Measure, Body
Muscle Strength
Range of Motion, Articular
Remyelination
Retention (Psychology)
Safety
Upper Extremity
Top products related to «Remyelination»
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Cuprizone is a laboratory equipment product manufactured by Merck Group. It is a chemical compound that is primarily used in research applications. The core function of Cuprizone is to induce demyelination in animal models, which is a condition where the protective myelin sheath around nerve fibers is damaged or lost.
Sourced in United States
Lysolecithin is a type of phospholipid molecule used in various laboratory applications. It is derived from lecithin, a common component of cell membranes. Lysolecithin is primarily used as a tool for studying membrane structure and function in biological research.
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Tamoxifen is a drug used in the treatment of certain types of cancer, primarily breast cancer. It is a selective estrogen receptor modulator (SERM) that can act as both an agonist and antagonist of the estrogen receptor. Tamoxifen is used to treat and prevent breast cancer in both men and women.
Sourced in United States, United Kingdom, Germany, Macao
Luxol fast blue is a staining dye commonly used in histological and neuroanatomical research. It is a soluble copper-based dye that selectively stains the myelin sheath of nerve fibers, allowing for the visualization and analysis of the myelination in tissue samples.
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The VT1000S is a vibratome, a precision instrument used for sectioning biological samples, such as tissues or organs, into thin slices for microscopic examination or further processing. The VT1000S provides consistent and accurate sectioning of samples, enabling researchers to obtain high-quality tissue sections for a variety of applications.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
Sourced in United States
Cuprizone is a chemical compound used in research applications. It is a copper-chelating agent that has been shown to induce demyelination in the central nervous system of rodents. The product is primarily used in the study of animal models of multiple sclerosis and other neurodegenerative diseases.
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GlutaMAX is a chemically defined, L-glutamine substitute for cell culture media. It is a stable source of L-glutamine that does not degrade over time like L-glutamine. GlutaMAX helps maintain consistent cell growth and performance in cell culture applications.
ImageJ 1.46m is an open-source image processing program designed for scientific multidimensional images. It provides a platform for the visualization, analysis, and processing of images.
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The L4129 is a piece of lab equipment designed for general laboratory use. It functions as a tool for performing various tasks and procedures within a laboratory setting. The core purpose of this product is to facilitate essential laboratory work, without making claims about its specific intended applications.
More about "Remyelination"
Remyelination is the vital process of restoring the myelin sheath, a protective layer around nerve fibers, after damage or loss.
This crucial mechanism allows for the recovery of efficient nerve signal transmission, essential for proper neurological function.
Remyelination research explores the biological pathways, therapies, and strategies to promote the regrowth of myelin in conditions like multiple sclerosis (MS), traumatic brain injury (TBI), and other demyelinating disorders.
The complex process of remyelination involves various factors, including oligodendrocyte precursor cells (OPCs), Cuprizone, Lysolecithin, Tamoxifen, and Luxol fast blue staining.
Researchers utilize techniques like VT1000S live imaging and ImageJ 1.46m analysis to study remyelination dynamics.
Therapies may incorporate Penicillin/streptomycin and GlutaMAX to support cell growth and regeneration.
By understanding the intricate remyelination mechanisms, scientists can develop innovative approaches to enhance the body's natural repair capabilities and improve outcomes for patients affected by these debilitating neurological conditions.
PubCompare.ai, the leading AI platform, can optimize remyelination research by locating the best protocols from literature, preprints, and patents, and using AI-driven comparisons to enhance reproducibility and accuracy, unlocking the power of data-driven insights to advance this critical field of study.
This crucial mechanism allows for the recovery of efficient nerve signal transmission, essential for proper neurological function.
Remyelination research explores the biological pathways, therapies, and strategies to promote the regrowth of myelin in conditions like multiple sclerosis (MS), traumatic brain injury (TBI), and other demyelinating disorders.
The complex process of remyelination involves various factors, including oligodendrocyte precursor cells (OPCs), Cuprizone, Lysolecithin, Tamoxifen, and Luxol fast blue staining.
Researchers utilize techniques like VT1000S live imaging and ImageJ 1.46m analysis to study remyelination dynamics.
Therapies may incorporate Penicillin/streptomycin and GlutaMAX to support cell growth and regeneration.
By understanding the intricate remyelination mechanisms, scientists can develop innovative approaches to enhance the body's natural repair capabilities and improve outcomes for patients affected by these debilitating neurological conditions.
PubCompare.ai, the leading AI platform, can optimize remyelination research by locating the best protocols from literature, preprints, and patents, and using AI-driven comparisons to enhance reproducibility and accuracy, unlocking the power of data-driven insights to advance this critical field of study.