Link between gum disease and Alzheimer's disease: A new perspective

🧠 𝗦𝘁𝗿𝗼𝗸𝗲 𝗶𝗻 𝘁𝗵𝗲 𝗬𝗼𝘂𝗻𝗴: 𝗔 𝗖𝗮𝗹𝗹 𝗳𝗼𝗿 𝗣𝗿𝗲𝗰𝗶𝘀𝗶𝗼𝗻 𝗮𝗻𝗱 𝗣𝗿𝗼𝘁𝗼𝗰𝗼𝗹 Stroke isn’t just a disease of aging. Increasingly, we’re seeing cerebrovascular events in patients under 50—often with devastating consequences. Unlike older adults, young stroke patients demand a broader differential and a deeper dive into underlying etiologies. 🔍 When a young adult presents with stroke symptoms, the protocol must go beyond the basics. We need to think autoimmune, hypercoagulable, and genetic. Here's a streamlined approach to the Young Stroke Protocol—a lab panel that helps uncover hidden culprits: 🧪 Autoimmune & Vasculitic Workup - ANA titer - Anti-ds DNA - Anti-CCP - ANCA (C & p) - ESR - C3 & C4 🧬 Thrombophilia & Coagulopathy Panel - Lupus anticoagulant - Anti-cardiolipin IgM & IgG - Anti-B2 glycoprotein IgM & IgG - Protein C & S - Antithrombin III Ab - Factor V Leiden mutation - Thrombophilia gene panel - Homocysteine 🎯 These labs aren’t just academic—they guide anticoagulation decisions, uncover systemic diseases like SLE or vasculitis, and help prevent recurrence. In young patients, stroke is often a symptom, not the diagnosis. Let’s shift the paradigm: from reactive to investigative, from age-based assumptions to precision medicine. If you're managing stroke in the young, what protocols or red flags do you prioritize? Let’s share and refine best practices. 🩺💬 #StrokeAwareness #YoungStroke #NeuroCriticalCare #Thrombophilia #AutoimmuneDisease #ClinicalProtocols #EvidenceBasedMedicine #ICU #EmergencyMedicine #Neurology #LinkedInMedEd

🧬 Getting the right diagnosis for progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) remains one of the biggest challenges patients face. These conditions are part of atypical Parkinsonism syndromes, sharing early symptoms with Parkinson's disease but having a completely different root cause. While Parkinson's and MSA result from alpha-synuclein protein buildup, PSP and CBD are primary tauopathies caused by tau protein dysfunction. 🧠 What is Tau Protein? Think of tau protein as the support system for your brain cells. It helps maintain microtubules - tiny highways that carry nutrients and critical information throughout brain cells. When tau works properly, your brain cells communicate seamlessly. But when tau malfunctions, it forms tangles that block these highways, disrupting communication and eventually causing brain cells to shut down. ⚕️ The Role of Tau Protein in PSP and CBD: The location where tau tangles form determines each disease's unique symptoms. In PSP, tau builds up in areas controlling movement, balance and thinking, leading to characteristic eye movement problems, balance difficulties and cognitive changes. Tau clumps found in brains with CBD cause asymmetric symptoms, typically starting on one side of the body with stiffness, shakiness and movement challenges. 🔬 Why Research on Tau Protein is Important: Scientists are making remarkable progress developing diagnostic breakthroughs like tau PET imaging to see tau patterns in living brains and biomarker tests using blood, spinal fluid and even skin samples. Treatment studies are testing therapies that prevent tau clumping and reverse existing buildup. This research offers hope for earlier diagnosis and more effective treatments, bringing us closer to better outcomes for everyone affected by these diseases. 📖 Read full article here: https://lnkd.in/eJAcz2Cf #TauProtein #PSP #CBD #Tauopathy #NeuroscienceResearch #BiomarkerResearch #PETImaging #RareDisease #NeurodegenerativeResearch #MedicalBreakthrough #HopeInAction #BecauseHopeMatters

Redefining Possibilities in CIDP Care. I had the privilege of interviewing Dr. Jeffrey Allen, a neurologist and neuromuscular specialist at the University of Minnesota, to discuss the evolving landscape of chronic inflammatory demyelinating polyneuropathy (CIDP), and the important work led by the GBS|CIDP Foundation Leadership Collaborative to establish standardized definitions for key clinical terms used in both patient care and clinical research. Dr. Allen shared his insights on: - The value of clear definitions for terms such as relapse, response, refractory, and remission. - How patient voices helped reshape the meaning of “refractory” to reflect hope and treatment potential. - Emerging research into inflammation, the complement system, and biomarkers that may transform how we understand and track disease activity. 📺 Watch the full interview here: https://lnkd.in/eZfMNvZi #CIDP #Neurology #PatientCentricity #ClinicalResearch #GBSCIDPFoundation #MedicalInnovation #RefractoryCIDP #AutoimmuneNeuropathy

A recent study from Wuhan University is challenging our long-standing understanding of Parkinson’s disease. Traditionally considered a neurodegenerative disorder originating in the brain, new evidence now suggests that the disease may, in fact, begin in the kidneys. Researchers identified abnormal aggregates of alpha-synuclein (α-Syn)—the same protein implicated in Parkinson’s pathology—within the renal tissue of patients diagnosed with the condition. These misfolded proteins are known to cause neurotoxicity when they accumulate in the brain. Interestingly, in preclinical animal models, intact renal function appeared to facilitate the clearance of α-Syn proteins. In contrast, compromised kidney function allowed these proteins to escape into systemic circulation, where they ultimately reached and affected the central nervous system. Even more compelling is the observation that individuals with chronic kidney disease—but without any neurological symptoms—also demonstrated α-Syn accumulation in their kidneys. This raises the possibility that renal tissue may serve as an early reservoir for pathological protein aggregation, potentially contributing to the subsequent neurodegenerative process seen in Parkinson’s. While these findings are preliminary and warrant further investigation, they open new avenues for early detection, risk stratification, and perhaps even prevention of Parkinson’s disease. Protecting and monitoring renal health may emerge as a crucial strategy in reducing neurodegenerative risk. #ParkinsonsBreakthrough #KidneyHealthMatters #NeuroScienceNews #FutureOfMedicine

A recent study from Wuhan University is challenging our long-standing understanding of Parkinson’s disease. Traditionally considered a neurodegenerative disorder originating in the brain, new evidence now suggests that the disease may, in fact, begin in the kidneys. Researchers identified abnormal aggregates of alpha-synuclein (α-Syn)—the same protein implicated in Parkinson’s pathology—within the renal tissue of patients diagnosed with the condition. These misfolded proteins are known to cause neurotoxicity when they accumulate in the brain. Interestingly, in preclinical animal models, intact renal function appeared to facilitate the clearance of α-Syn proteins. In contrast, compromised kidney function allowed these proteins to escape into systemic circulation, where they ultimately reached and affected the central nervous system. Even more compelling is the observation that individuals with chronic kidney disease—but without any neurological symptoms—also demonstrated α-Syn accumulation in their kidneys. This raises the possibility that renal tissue may serve as an early reservoir for pathological protein aggregation, potentially contributing to the subsequent neurodegenerative process seen in Parkinson’s. While these findings are preliminary and warrant further investigation, they open new avenues for early detection, risk stratification, and perhaps even prevention of Parkinson’s disease. Protecting and monitoring renal health may emerge as a crucial strategy in reducing neurodegenerative risk. #ParkinsonsBreakthrough #KidneyHealthMatters #NeuroScienceNews #FutureOfMedicine

☑️ *READ DESCRIPTION BELOW:* Part 1: Overview of Bone marrow adipocytes in disease pathology. (1) Hematopoietic diseases: BMAs enhance adipogenesis (regulated by GATA2, AdipoQ, PPAR-γ), remodel the microenvironment via GDF15 and CXCL12, and secrete FFAs and leptin, driving disease progression. (2) Bone malignancies: Adipocytes recruit tumor-associated macrophages via CCL2 and engage in bidirectional crosstalk with cancer cells through metabolites, adipokines, and cytokines, promoting proliferation, invasion, and chemoresistance. (3) Endocrine disorders and anorexia nervosa: Pituitary dysfunction reduces GH and estrogen, impairing BMA function. Anorexia nervosa upregulates Pref-1 and downregulates IGF-I, contributing to metabolic dysregulation. (4) Cardiovascular diseases: Myocardial ischemia decreases adiponectin and SFRP5, altering adipocyte function. BMAs also influence atherosclerosis through adipokine secretion (adiponectin, omentin) and cholesterol metabolism(...) Fan Y, Front Cell Dev Biol. 2025 Aug 7;13:1633801. doi: 10.3389/fcell.2025.1633801. PMID: 40852589; PMCID: PMC12367753. #Gesundheit #Bildung #Fuehrung #Coaching #Mindset #Motivation #Gehirn #Neuroscience #Psychologie #Persoenlichkeitsentwicklung #Kindheit #KeyNoteSpeaker #Humangenetik #Biochemie #Neuroleadership #Ernaehrung #Transformation #Stress #Demografie #Gender #Age #interkulturelleKompetenz #Epigenetik #Veraenderung #EmotionaleIntelligenz #Change #Gesellschaft #Organisationsentwicklung #Philosophie #Beratung # Quantum

The visual and functional impairment in the eyes of patients with optic neuritis caused by anti-aquaporin 4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (#NMOSD) is more severe than in patients with anti-myelin-oligodendrocyte-glycoprotein-associated disease (#MOGAD) and correlates with structural loss, according to a study published in the journal Multiple Sclerosis and Related Disorders. Read more: https://bit.ly/41honyJ #RareDisease #OpticNeuritis #AQP4 #Neurology

Our latest paper has been published in Science Advances. In spinal muscular atrophy (SMA), it is well-established that spinal motor neurons lose excitatory inputs early in the disease. Our new study shows that, in parallel, these neurons also come under increased inhibitory drive. This dual mechanism, reduced excitation and heightened inhibition, helps explain why muscles are not properly recruited in SMA. Our findings point to a therapeutic window: early pharmacological interventions that both increase excitability and limit inhibitory drive may improve movement outcomes for children with SMA. https://lnkd.in/g_KJwafE https://www.mentislab.org/ #SpinalMuscularAtrophy #MotorNeurons #Neurodegeneration #ChildHealth

A promising breakthrough in Alzheimer’s research reveals that the translocator protein 18 kDa (TSPO), a marker of neuroinflammation, rises in key brain regions decades before symptoms appear. This discovery by Florida International University scientists highlights TSPO, expressed primarily by microglia, as an early and sensitive biomarker detectable through advanced brain imaging. It opens the door to earlier diagnosis and targeted therapeutic strategies to potentially delay or prevent cognitive decline, shifting the paradigm from symptom management to prevention. These findings pave the way for novel personalized interventions that could improve quality of life for millions at risk of Alzheimer’s disease. https://lnkd.in/ggm58TFg

Epigenetics & cardiology 🧬🫀 Interesting new research suggests that only a fraction of patients exposed to group-A strep develop rhematic heart valve disease, possibly due to genetic and epigenetic factors. Multi-omics approaches may help us discover why. As clinicians and data scientists, we should harness these insights to improve early diagnosis and personalise treatment. #Cardiology #Epigenetics #DataScience