NIH Clinical Center (CC)’s Post

🧠 A Unique Intersection of Neurology and Infectious Diseases and the challenges assosiated with it🌍 Recently, I encountered a thought-provoking case that tested the boundaries of clinical insight and interdisciplinary care. A 44-year-old woman, living with HIV and presenting with progressive neurological symptoms, was diagnosed with cerebral toxoplasmosis and HIV-associated demyelination based on distinct findings on MRI. The case underscored the challenges of managing severe immunosuppression and opportunistic infections. Multiple ring-enhancing lesions with surrounding edema pointed to cerebral toxoplasmosis, while diffuse white matter hyperintensities hinted at the coexisting HIV-associated white matter damage. Through targeted therapy, combining pyrimethamine, sulfadiazine, and antiretroviral management, we were able to stabilize her condition, offering a glimpse of hope in a complex clinical scenario. This case was not just a reminder of the critical need for adherence to antiretroviral therapy but also a testament to the importance of multidisciplinary collaboration. The detailed case report, now published in a leading medical journal, aims to educate and inspire clinicians worldwide to remain vigilant in managing such dual-pathology cases. It’s moments like these that remind me why I chose this field—to solve intricate puzzles, provide compassionate care, and contribute to the growing body of medical knowledge. 🔗 Always learning, always growing! 🌟 #Neurology #InfectiousDiseases #CerebralToxoplasmosis #HIVCare #MedicalResearch #CaseStudyInsights #HealthcareInnovation

Deferiprone, an iron-chelating agent, accelerates cognitive decline and frontal brain atrophy after 12-months of 'treatment' in Alzheimer´s disease patients. It has shown to be detrimental, even though some previous trials in Parkinson´s were mostly (but not entirely) positive. Iron is important to the brain as a cofactor in numerous neuronal processes, of which neurotransmitter production (dopamine, norepinephrine). Anti-amyloid immunization therapies also showed redistribution of the iron trapped within plaques. So what about the brain rust and amyloid pathology as some studies suggest (redox of iron, iron becoming more reactive in presence of oxygen)? Or was the dosage of deferiprone simply too high? Is taking iron away from the 🧠 just too simple of an hypothesis, similar as it is with plaque removal approaches, to battle Alzheimer's? Interesting results! #Alzheimer #treatment #iron #brain

Traumatic Brain Injury (TBI) is a risk factor for ALZHEIMER’S DISEASE (AD) and other dementias and neurodegenerative disorders. We are pleased to be working with Dr Aylin Reid to evaluate indoleamine 2,3-dioxygenase (IDO) enzyme inhibition as a therapeutic target to improve cognitive and behavioural outcomes after traumatic brain injury. The development of IDO inhibitors is a pursuit of ongoing interest in my laboratory (See: https://lnkd.in/gUYaujRA; https://lnkd.in/g9UmjKtS).  Dr Reid’s study supports a role for IDO in the injury mechanisms and outcomes of TBI. IDO activity is transiently increased after TBI and can be targeted to improve behavioural outcomes. As IDO activity is mainly a result of pathological conditions, this may be a helpful target to improve outcomes with minimal side-effects after TBI. This proof of principle study demonstrates further work in this area is warranted (moreover, given that TBI is a risk factor for AD, this study also opens a consideration of agents to ameliorate AD risk factors).     Read here (open access): https://lnkd.in/gJuxKZCk     #alzheimerdisease, #dementia, #neurodegeneration, #drugdesign, #immunology  

Brain and cognitive changes in patients with long COVID compared with infection-recovered control subjects🧠💡 From Brain, April 2024: In the wake of the global pandemic, the phenomenon of Long COVID has emerged as a significant concern, affecting between 2.5% to 28% of individuals who have contracted SARS-CoV-2. Characterized by the persistence of symptoms months after the initial illness, Long COVID presents a myriad of health challenges, particularly in the neurological domain. However, the specific brain changes underlying these neuropsychological impairments have remained elusive, until now. A pioneering study has made strides in demystifying the cognitive and neurological repercussions of Long COVID. The research involved a cohort of 83 patients still grappling with neurological symptoms post-COVID-19, alongside 22 healthy controls who had recovered from the virus without enduring neurological aftereffects. This carefully matched group, in terms of age, sex, and educational level, underwent a battery of assessments, including clinical interviews, a suite of standardized neuropsychological tests, and structural MRI scans. The findings are revealing. The average global cognitive function in Long COVID patients, as gauged by the ACE III screening test, was significantly lower than that of the recovered controls. Notably, nearly half of the Long COVID patients exhibited deficits in episodic memory, with a significant portion also showing impairments in key cognitive domains such as attention, working memory, processing speed, and verbal fluency. The study's neuroimaging component offered further insights. MRI analyses indicated that Long COVID patients had a thinner cortex in regions centered around the left posterior superior temporal gyrus, compared to their recovered counterparts. Moreover, these patients showed signs of altered brain connectivity, with lower fractional anisotropy and higher radial diffusivity in extensive areas of the cerebral white matter. Crucially, the research unveiled a clear correlation between cognitive impairments and brain abnormalities. The altered connectivity in white matter regions was linked to deficits in episodic memory, overall cognitive function, attention, and verbal fluency. Link: https://lnkd.in/gMT6Cmsk #LongCOVID #Neurology #CognitiveHealth #COVID19Research #BrainScience #PandemicRecovery 🌍🔬🧬

🧠 Very interesting study by Shapiro et al., 2024 evaluates the association between youth-onset diabetes (Y-DM) and early signs of neurodegeneration and Alzheimer’s disease (AD) using data from the SEARCH for Diabetes in Youth study. It demonstrates significant differences in plasma biomarkers for neurodegeneration and AD neuropathology in adolescents and young adults with Y-DM compared to controls, highlighting an early onset of neuropathological changes. 🔬 Study Design: The study analyzed plasma biomarkers and conducted PET scans to measure brain amyloid and tau densities in AD-sensitive brain regions among participants with Y-DM and age-matched controls. Both cross-sectional and longitudinal analyses were employed. 💡 Key findings: 🕐 Plasma levels of Aβ40 and Aβ42 were significantly lower, while pTau181 was higher in Y-DM participants during adolescence and young adulthood compared to controls (p < 0.05 in adolescence, p < 0.001 in adulthood). 🕑 Longitudinal analysis showed significant increases in GFAP and NfL levels from adolescence to adulthood in Y-DM participants (p < 0.01), suggesting progressive neurodegeneration. 🕒 Correlational analysis indicated that changes in plasma levels of biomarkers were associated with fluid cognitive scores in adulthood (positive correlation for Aβ42, p = 0.04; negative correlation for pTau181 approaching significance, p = 0.05). For more details: https://lnkd.in/d-k5f2rP #YouthOnsetDiabetes #Neurodegeneration #AlzheimersDisease #Biomarkers #CognitiveHealth

DIFFERENT approach to ADDRESSING Neurodegenerative Diseases? 🔹 Glia cells, also called glial or neuroglial, are non-neuronal cells in the CNS and peripheral nervous system but do not produce electrical impulses. 🔹 The neuroglia make up more than one-half the volume of neural tissue in the human body. Their functions include: ▪️maintain homeostasis ▪️form myelin in the peripheral nervous system ▪️provide support and protection for neurons. 🔹 Three primary neuroglia are: ▪️ microglia ▪️ astrocytes ▪️ oligodendrocytes Of these three, microglia are the primary innate, immune cells of the CNS and it is the primary responder to b-amyloid plaque. Further, microglia are the resident cells of the brain that regulate brain development, maintenance of neural networks, and injury repair. 🔺 Activation of microglia and the presence of neuroinflammation are pathological hallmarks of neurodegenerative diseases. 🔺 The characterization of microglia can be a kind of “Dr. Jekyll & Mr. Hyde.” 🔺 Ameliorating the development & progression of neurodegenerative diseases could involve shifting the brain’s own immune cells (microglia) from an aggressive, pro-inflammatory state to a neuroprotective state. 💡 This will help treat a broad array of diseases. For example, upon activation microglia clear amyloid —beginning pathology of Alzheimer’s disease. But during this process of eliminating amyloid the microglia cause inflammation. 🔑 Neuronal reprogramming via epigenetic modifications could play a part in getting the microglia to go from being a “killer” which causes inflammation back to being a good “housekeeper” where they are clearing amyloid while you sleep & when induced by energy (natural) foods. There is on-going research studying the significance of re-programming glial cells to ameliorate neurological diseases… CLICK LINK below 👇🏾in the COMMENT Section for a recent publication on therapeutic potential. STAY TUNED for more science-based evidence of #precisionmedicine As always, I look forward to your contribution in elevating the dialogue. #alzheimers #data #medicine #innovation Alzheimer's Disease Data Initiative Alzheimer's Association®

🔍 Study Reveals Neurotrophins as Key Targets Against Neurodegenerative Diseases 🧠✨ A recent systematic review underscores the vital role of neurotrophins in the fight against neurodegenerative disorders such as Alzheimer’s and Parkinson’s. This comprehensive analysis, adhering to PRISMA 2020 guidelines, evaluated over 3,000 studies and spotlighted 15 significant research pieces from the past decade. 🌟 Key Insights: - Neurotrophins enhance brain resilience by supporting neuroplasticity and promoting neurogenesis. - Understanding their intricate signaling pathways is crucial for identifying intervention points to slow disease progression. - While current clinical trials show promise, more extensive research is essential to validate findings and tackle delivery challenges. The exploration of neurotrophins as therapeutic agents opens exciting avenues for mitigating the impacts of these debilitating diseases. 👉 Discover more about this groundbreaking study by clicking on the link! #Alzheimers #BrainHealth #MedicalResearch #NeurodegenerativeDiseases #Neurotrophins #Parkinsons #Publications #MarketAccess #MarketAccessToday

A traumatic brain injury, or TBI, is caused by a contusion to the head that may result in injury to the brain. This type of injury combined with the inherited genetic risk factors can result in the accelerated development of Alzheimer’s disease and related dementia, or ADRD. https://lnkd.in/enD78Pqp #alzheimers #braininjury #TBI #brainhealth #dementia #ADRD #riskfactors #alzfdn

🧠🔍 #GuillainBarreSyndrome | A rare, rapidly progressive neurological disease that causes muscle weakness and eventually paralysis. 🔍🧠 Guillain Barré syndrome (GBS) is an autoimmune disorder. In GBS, the immune system specifically attacks the nerves. GBS is usually triggered by a viral or bacterial infection. Rarely, viral or bacterial components (proteins) can appear to look similar to your body’s proteins. When this happens, the immune system becomes confused and starts to attack its own body. When the nerves are attacked by the immune system, this can result in GBS. GBS isn't contagious and it's not passed down through families (it is not an inherited disease). Diagnosis of GBS is based on the patient history, neurological electrophysiological, and cerebrospinal fluid (CSF) examinations. Although most patients with GBS recover spontaneously, all of them need to be hospitalized for disease-modifying immunotherapy and multispecialty supportive care because of the unpredictable, potentially life-threatening and severely disabling course of GBS. 💪✨ Raising awareness about Guillain-Barré syndrome can help with early diagnosis and improve outcomes. For more information and support resources, visit our website @ https://lnkd.in/geS8EyW7 #NeurologicalDisorder #AutoimmuneDisease #EarlyDetection #HealthAwareness #MedicalCare #RareDisease #Neurology #PatientSupport #RecoveryJourney #WellnessJourney #GuillainBarreSyndromeSymptoms #GuillainBarreSyndromeCauses #GuillainBarreSyndromeDiagnosis #GuillainBarreSyndromeManagement #GuillainBarreSyndromeTreatment #Bhimar #LifeSciences #Healthcare 

Study finds significant overlap in neurochemicals from long COVID and ME/CFS patients The National Centre for Neuroimmunology and Emerging Diseases (NCNED) at Griffith University continues to build upon its novel discoveries in long COVID and Myalgic Encephalomyelitis, also known as Chronic Fatigue Syndrome (ME/CFS). Researchers at NCNED directly compared brain neurochemical levels in long COVID and ME/CFS patients with healthy controls using MRI. The study’s first author Dr Kiran Thapaliya said “People with long COVID and ME/CFS have significantly elevated neurochemical levels, compared with healthy controls potentially causing multiple symptoms in both conditions. “Long COVID and ME/CFS have a remarkably similar neurochemical signature, providing further evidence for a significant link between the two conditions. “This novel study reveals the level of neurochemicals in the brain were associated with symptoms such as cognitive impairment, unrefreshing sleep, pain, and physical limitation in long COVID and ME/CFS patients.” Director of the NCNED, Professor Sonya Marshall-Gradisnik, said: “These findings build upon our published novel findings in ME/CFS and long COVID. “These latest findings published in the American Journal of Medicine, provide greater insight into how neurochemicals may play a key role in the development and progression of these conditions. “The NCNED has a critical mass of exceptionally talented researchers and clinicians who are committed to these patients. “We are incredibly fortunate to have access to state-of-the-art technologies that enable us to produce wonderful scientific discoveries. “We are uniquely positioned internationally to undertake scientific laboratory and MRI research in long COVID and ME/CFS in tandem, and monitor the health and economic impact of the patients as well as undertake clinical trials.” The study ‘Imbalanced Brain Neurochemicals in long COVID and ME/CFS: A Preliminary Study using MRI’ has been published in the American Journal of Medicine. Posted by Larry Cole