Yulia Ilina’s Post

🧠 A new study shows (yet again) the significant role of increased blood-brain barrier (BBB) permeability in the pathogenesis of Alzheimer’s Disease (AD). The research demonstrates how chronic extravasation of bloodborne amyloid-beta (Aβ)42 peptide and brain-reactive autoantibodies, facilitated by a permeable BBB, contribute to cognitive impairments and AD-related pathological changes in a mouse model. 💡 Key findings: 1.   Mice subjected to chronic BBB permeability showed marked deficits in long-term memory retention and heightened susceptibility to cognitive interference, spotlighting the intricate interplay between BBB integrity and cognitive health. 2.   Immunohistochemical analyses revealed an increased influx of Aβ42 and IgG into the brain, with selective binding to neurons. This suggests a crucial pathway through which bloodborne factors contribute to neuronal dysfunction. 3.   The study underscores the potential synergistic effects of BBB compromise and the entry of Aβ42 into the brain in initiating the neuropathological and cognitive changes associated with AD. Check out for more: https://lnkd.in/dKGq6zNr #AlzheimersResearch, #BloodBrainBarrier, #Neuroscience, #CognitiveHealth, #AmyloidBeta, #BrainHealth, #Neurodegeneration

🧠 Recent research offers new pathways for diagnostics and therapeutic strategies in Alzheimer's disease (AD) through a deeper understanding of amyloid plaques' chemical makeup. This study systematically characterizes the metal accumulation within these plaques, which could be crucial for developing future treatments and diagnostic tools. 🔬 Methodology: Utilizing Synchrotron X-ray Spectromicroscopy, the research provides a label-free, nanoscale chemical analysis of amyloid plaques in human AD tissue. This innovative approach relies on a specific C−H carbon absorption feature to distinguish amyloid plaques from surrounding tissues, enabling precise chemical analysis without modifying the sample's native chemistry. 💡 Key Results: 1️⃣ Amyloid plaques have higher concentrations of calcium, carbonates, and iron compared to adjacent brain tissue. 2️⃣ Low-oxidation-state iron phases, including ferromagnetic metallic iron, were identified within the plaques. 3️⃣ The detection of ferromagnetic iron in intact tissue sections suggests its role in increasing the redox burden, potentially contributing to neurodegeneration in AD. Read the full paper here: https://lnkd.in/dVn9Cvsj #AlzheimersResearch #Neuroscience #AmyloidPlaques #SynchrotronXray #Neurodegeneration

Roche Strikes Again! "After a year of treatment, our BTK inhibitor fenebrutinib was able to suppress nearly all disease activity and disability progression in people with multiple sclerosis," said Levi Garraway, M.D., Ph.D., Roche’s Chief Medical Officer. This could be a major breakthrough in MS treatment, as 96% of patients in the OLE period were relapse-free, with a remarkable 0.04 annualized relapse rate (ARR). MRI results also showcased 99% reduction in active inflammation and a threefold decrease in chronic disease burden. With promising ongoing Phase III trials, fenebrutinib may soon reshape the future of MS care! Stay tuned for more in 2025. #MultipleSclerosis #Neuroscience #RocheInnovation #Fenebrutinib #ClinicalResearch #Pharma

Build up of amyloid beta and tau proteins in the brain leads to neurodegeneration and cognitive impairment associated with Alzheimer's disease. While amyloid beta forms the plaques linked to the disease, its soluble monomers have a more detrimental impact on healthy brain function. Tau forms insoluble filaments that accumulate as neurofibrillary tangles and causes the internal skeleton of neurons to fall a part. Early diagnosis relies on identifying these biomarkers. Testing for specific biomarkers in the cerebral spinal fluid is one of the most accurate diagnostic tests for Alzheimer's. However, this method is more invasive than blood tests, requiring a painful spinal tap procedure, costs 2 to 3 times more than blood tests, and is difficult to scale for testing new disease-modifying treatments. ALZpath recently released results of their blood-based biomarker assay, representing a significant advancement. This novel detection method demonstrates high diagnostic accuracy and consistency in identifying elevated amyloid beta and tau. Hopefully, this will be an accessible tool for health care providers worldwide in the early diagnosis and treatment of Alzheimer's Disease. #AlzheimersDisease #Dementia #Neuroscience #Diagnostics #MedicalAccessibility #MedicalBreakthrough #Biomarkers Link to article in the comments

Vol. 23 / Iss. 4 #JIN #OpenAccess #ResearchPapers #neuroscience "Changes in SLITRK1 Level in the Amygdala Mediate Chronic Neuropathic Pain-Induced Anxio-Depressive Behaviors in Mice" 📋 Full text: https://lnkd.in/gpZ5gTJ8 #amygdala #depressive #Behaviors #pain Journal of Integrative Neuroscience Abstract Background: Comorbid chronic neuropathic pain (NPP) and anxio-depressive disorders (ADD) have become a serious global public-health problem. The SLIT and NTRK-like 1 (SLITRK1) protein is important for synaptic remodeling and is highly expressed in the amygdala, an important brain region involved in various emotional behaviors. We examined whether SLITRK1 protein in the amygdala participates in NPP and comorbid ADD. Methods: A chronic NPP mouse model was constructed by L5 spinal nerve ligation; changes in chronic pain and ADD-like behaviors were measured in behavioral tests. Changes in SLITRK1 protein and excitatory synaptic functional proteins in the amygdala were measured by immunofluorescence and Western blot. Adeno-associated virus was transfected into excitatory synaptic neurons in the amygdala to up-regulate the expression of SLITRK1. Results: Chronic NPP-related ADD-like behavior was successfully produced in mice by L5 ligation. We found that chronic NPP and related ADD decreased amygdalar expression of SLITRK1 and proteins important for excitatory synaptic function, including Homer1, postsynaptic density protein 95 (PSD95), and synaptophysin. Virally-mediated SLITRK1 overexpression in the amygdala produced a significant easing of chronic NPP and ADD, and restored the expression levels of Homer1, PSD95, and synaptophysin. Conclusion: Our findings indicated that SLITRK1 in the amygdala plays an important role in chronic pain and related ADD, and may prove to be a potential therapeutic target for chronic NPP-ADD comorbidity.

Inflammed Brain— Chronic inflammation within the gut can be preceded by inflammation in the brain. Part of this reasoning results from low vagal tone. (Vagus nerve stimulates the release of digestive enzymes and gastric acid, promoting efficient digestion— this starts in the brain) #braingutconnection Vagus nerve stimulation (VNS), whether invasive or non-invasive, has emerged as a promising intervention in the field of Bioelectronic Medicine. VNS involves delivering electrical impulses to the VN, which can modulate its activity and thus influence inflammatory processes. The advantage of VNS lies in its ability to target specific neural pathways with minimal side effects compared to traditional pharmacological treatments that can trigger unfavorable side effects in the gut and liver. References: Bonaz B, Sinniger V and Pellissier S (2017) The Vagus Nerve in the Neuro-Immune Axis: Implications in the Pathology of the Gastrointestinal Tract. Front. Immunol. 8:1452. doi: 10.3389/fimmu.2017.01452 #functionalsportsmedicine #neuroimmunology #braingutaxis #gutbrainaxis #bioenergetics

#macrophages #neuroinflammation #alzheimer Apolipoprotein E variant ApoE4 has been well characterized as a major risk factor for Alzheimer disease and for damages to the white matter associated with vascular dementia. Yet, the mechanisms by which ApoE4 promotes brain damages are not fully understood. This paper in Nature Neuroscience highlights the key role of ApoE4-expressing border-associated macrophages (BAMs) in vascular and brain tissue damages, via enhanced inflammation (production of reactive oxygen species). Removing BAMs or decreasing their expression of ApoE4 each diminishes the level of vascular impairment, showing that BAMs are both the source and the effectors of ApoE4-related damages. Find out more about these findings here ⬇ https://lnkd.in/e-kSjfyH

I am excited to share my first first-author paper, "Insulin restores retinal ganglion cell functional connectivity and promotes visual recovery in glaucoma" recently published in the Science Advances journal. The study investigates how daily insulin eye drops can stimulate the regrowth of dendrites and synapses in retinal ganglion cells (RGCs) during ocular hypertension. Our results suggest that insulin could be a promising pro-regenerative strategy with potential clinical applications for managing glaucoma and other neurodegenerative diseases characterized by dendritic and synaptic pathology. We're excited about the therapeutic implications of this work and look forward to further advancing this line of research. You can read the full article here: https://lnkd.in/eV4GYQrV I welcome any questions or discussion about the findings and their significance. Feel free to share your thoughts in the comments. #neuroscience #neurodegeneration #glaucoma #neuroprotection #neuroregenerative #insulin #dendrites #RGCs

What do Major Depressive Disorder and the cerebral vasculature have to do with one another? Here are 5 things I recently learned: 1) Clinical and preclinical data suggest that brain blood vessels are more permeable in MDD patients and animal models of MDD. 2) Brain blood vessel permeability is especially pronounced in brain areas typically associated with pleasure and reward. 3) Molecules released from cells that make up brain blood vessels can regulate and prevent death of neurons, especially during stressful conditions. 4) Researchers think trophic factors (molecules responsible for cell reproduction and growth, e.g. BDNF) may explain the therapeutic activity of antidepressants. 5) Cells that make up brain blood vessels may be a source of trophic factors able to prevent neuron death during stressful conditions. What are your thoughts? Had you previously heard of the involvement of the cerebral vasculature in MDD? Could BBB targeted drugs prove beneficial toward developing new antidepressants? #Research #ScienceCommunication #Neuroscience #BloodBrainBarrier #MentalHealth #BBBResearch Sources: 1) Menard C, Pfau ML, Hodes GE, et al. Social stress induces neurovascular pathology promoting depression. Nat Neurosci. 2017;20(12):1752-1760. doi:10.1038/s41593-017-0010-3 2) Guo S, Som AT, Waeber C, Lo EH. Vascular neuroprotection via TrkB- and Akt-dependent cell survival signaling. In: Journal of Neurochemistry. Vol 123. J Neurochem; 2012:58-64. doi:10.1111/j.1471-4159.2012.07944.x 3) Casarotto PC, Girych M, Fred SM, et al. Antidepressant drugs act by directly binding to TRKB neurotrophin receptors. Cell. 2021;184(5):1299-1313.e19. doi:10.1016/j.cell.2021.01.034

Promising news for PwMS with #multiplesclerosis (MS) ! Non-Invasive Therapy to Promote "Repair" and "Remyelination" in MS  Researchers find that a non-drug based treatment approach called acute intermittent hypoxia (AIH), which consists of short periods of reduced oxygen, reduces inflammation, protects nerve fibres, and promotes repair in mice with multiple sclerosis-like disease. In MS, Myelin - the protective covering of nerve fibers in the brain , becomes damaged or lost. Effective therapies that promote myelin production (or remyelination) are needed for MS. In a recent study , Dr. Valerie M. K. Verge (University of Saskatchewan) and team aimed to examine whether an emerging non-invasive treatment approach, called AIH  could be used for MS to promote repair and remyelination. AIH treatment consists of alternating amounts of low oxygen (11% oxygen) and normal oxygen (21% oxygen) over a short period of time. In this study, mice with MS-like disease received AIH treatment for seven days and were compared to a group that received normal levels of oxygen in place of treatment. The researchers found that AIH treatment significantly enhanced repair processes in mice with MS-like disease. Treated mice showed improved clinical disease scores, reduced inflammation, enhanced remyelination, and increased protection of nerve fibres. Some of these improvements lasted up to two weeks following treatment. There was also an increase in myelin-producing cells- oligodendrocytes, and the cells that generate oligodendrocytes, called oligodendrocyte precursor cells (or OPCs), in areas of damage. Overall, the results suggest AIH treatment may be promoting an environment supportive of repair and remyelination. While the findings of this study are promising, further research will need to assess whether this treatment has the same effect in people with MS. #msresearch #neuroscience #msawarnessweek #TheMSPharmacist