186 results found
Edison P, 2021, Call for Papers: Brain Connectivity., Brain Connect
Pascoal TA, Benedet AL, Ashton NJ, et al., 2021, Microglial activation and tau propagate jointly across Braak stages, NATURE MEDICINE, ISSN: 1078-8956
Edison P, 2021, Call for Papers: Brain Connectivity., Brain Connect
Edison P, 2021, Brain Connectivity: Neuronal Damage in COVID-19, BRAIN CONNECTIVITY, Vol: 11, Pages: 405-407, ISSN: 2158-0014
Mallon DH, Malhotra P, Naik M, et al., 2021, The role of amyloid PET in patient selection for extra-ventricular shunt insertion for the treatment of idiopathic normal pressure hydrocephalus: A pooled analysis., J Clin Neurosci, Vol: 90, Pages: 325-331
BACKGROUND: Idiopathic Normal Pressure Hydrocephalus (iNPH) can be effectively treated through shunt insertion. However, most shunted patients experience little or no clinical benefit, which suggests suboptimal patient selection. While contentious, multiple studies have reported poorer shunt outcomes associated with concomitant Alzheimer's disease. Prompted by this observation, multiple studies have assessed the role of amyloid PET, a specific test for Alzheimer's disease, in patient selection for shunting. METHODS: A comprehensive literature search was performed to identify studies that assessed the association between amyloid PET result and the clinical response to shunting in patients with suspected iNPH. Pooled diagnostic statistics were calculated. RESULTS: Across three relevant studies, a total of 38 patients with suspected iNPH underwent amyloid PET imaging and shunt insertion. Twenty-three patients had a positive clinical response to shunting. 18/28 (64.3%) of patients with a negative amyloid PET and 5/10 (50%) with a positive amyloid PET had a positive response to shunting. The pooled sensitivity, specificity and accuracy was 33.3%, 76.2% and 58.3%. None of these statistics reached statistical significance. CONCLUSION: The results of this pooled analysis do not support the selection of patients with suspected iNPH for shunting on the basis of amyloid PET alone. However, due to small cohort sizes and weakness in study design, further high-quality studies are required to properly determine the role of amyloid PET in assessing this complex patient group.
Crook H, Raza S, Nowell J, et al., 2021, Long covid-mechanisms, risk factors, and management., BMJ, Vol: 374, Pages: 1-18, ISSN: 1759-2151
Since its emergence in Wuhan, China, covid-19 has spread and had a profound effect on the lives and health of people around the globe. As of 4 July 2021, more than 183 million confirmed cases of covid-19 had been recorded worldwide, and 3.97 million deaths. Recent evidence has shown that a range of persistent symptoms can remain long after the acute SARS-CoV-2 infection, and this condition is now coined long covid by recognized research institutes. Studies have shown that long covid can affect the whole spectrum of people with covid-19, from those with very mild acute disease to the most severe forms. Like acute covid-19, long covid can involve multiple organs and can affect many systems including, but not limited to, the respiratory, cardiovascular, neurological, gastrointestinal, and musculoskeletal systems. The symptoms of long covid include fatigue, dyspnea, cardiac abnormalities, cognitive impairment, sleep disturbances, symptoms of post-traumatic stress disorder, muscle pain, concentration problems, and headache. This review summarizes studies of the long term effects of covid-19 in hospitalized and non-hospitalized patients and describes the persistent symptoms they endure. Risk factors for acute covid-19 and long covid and possible therapeutic options are also discussed.
Calsolaro V, Matthews PM, Donat CK, et al., 2021, Astrocyte reactivity with late onset cognitive impairment assessed in-vivo using 11C-BU99008 PET and its relationship with amyloid load, Molecular Psychiatry, ISSN: 1359-4184
11C-BU99008 is a novel positron emission tomography (PET) tracer that enables selective imaging of astrocyte reactivity in vivo. To explore astrocyte reactivity associated with Alzheimer’s disease, 11 older, cognitively impaired (CI) subjects and 9 age-matched healthy controls (HC) underwent 3T magnetic resonance imaging (MRI), 18F-florbetaben and 11C-BU99008 PET. The 8 amyloid (Aβ)-positive CI subjects had higher 11C-BU99008 uptake relative to HC across the whole brain, but particularly in frontal, temporal, medial temporal and occipital lobes. Biological parametric mapping demonstrated a positive voxel-wise neuroanatomical correlation between 11C-BU99008 and 18F-florbetaben. Autoradiography using 3H-BU99008 with post-mortem Alzheimer’s brains confirmed through visual assessment that increased 3H-BU99008 binding localised with the astrocyte protein glial fibrillary acid protein and was not displaced by PiB or florbetaben. This proof-of-concept study provides direct evidence that 11C-BU99008 can measure in vivo astrocyte reactivity in people with late-life cognitive impairment and Alzheimer’s disease. Our results confirm that increased astrocyte reactivity is found particularly in cortical regions with high Aβ load. Future studies now can explore how clinical expression of disease varies with astrocyte reactivity.
Edison P, Mallon DH, 2021, The role of amyloid PET in patient selection for extra-ventricular shunt insertion for the treatment of idiopathic normal pressure hydroephalus: A pooled analysis ., Journal of Clinical Neuroscience, ISSN: 0967-5868
Edison P, 2021, Microglial activation and blood-brain barrier leakage: chicken and egg?, Brain, Vol: 144, Pages: 1284-1285
Alagaratnam J, von Widekind S, De Francesco D, et al., 2021, Correlation between CSF and blood neurofilament light chain protein: A systematic review and meta-analysis, BMJ Open Neurology, Vol: 3, ISSN: 2632-6140
Objective To assess the overall pooled correlation coefficient estimate between cerebrospinal fluid (CSF) and blood neurofilament light (NfL) protein.Methods We searched Medline, Embase and Web of Science for published articles, from their inception to 9 July 2019, according to Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. Studies reporting the correlation between CSF and blood NfL in humans were included. We conducted a random-effects meta-analysis to calculate the overall pooled correlation coefficient estimate, accounting for correlation technique and assay used. Heterogeneity was assessed using the I2 statistic test. In sensitivity analyses, we calculated the pooled correlation coefficient estimate according to blood NfL assay: single-molecule array digital immunoassay (Simoa), electrochemiluminescence (ECL) assay or ELISA.Results Data were extracted from 36 articles, including 3961 paired CSF and blood NfL samples. Overall, 26/36 studies measured blood NfL using Simoa, 8/36 ECL, 1/36 ELISA and 1 study reported all three assay results. The overall meta-analysis demonstrated that the pooled correlation coefficient estimate for CSF and blood NfL was r=0.72. Heterogeneity was significant: I2=83%, p<0.01. In sensitivity analyses, the pooled correlation coefficient was similar for studies measuring blood NfL using Simoa and ECL (r=0.69 and r=0.68, respectively) but weaker for ELISA (r=0.35).Conclusion Moderate correlations are demonstrated between CSF and blood NfL, especially when blood NfL was measured using Simoa and ECL. Given its high analytical sensitivity, Simoa is the preferred assay for measuring NfL, especially at low or physiological concentrations, and this meta-analysis supports its use as the current most advanced surrogate measure of CSF NfL.PROSPERO registration number CRD42019140469
Edison P, 2021, Brain Connectivity and Neurological Sequalee in COVID-19, Brain Connectivity
Edison P, 2021, Brain Connectivity and Neurological Sequalae in COVID-19, BRAIN CONNECTIVITY, Vol: 11, Pages: 331-332, ISSN: 2158-0014
Edison P, 2021, Microglial activation and blood-brain barrier leakage: chicken and egg?, Brain
Edison P, 2021, Brain Connectivity and COVID-19, Brain Connectivity, ISSN: 2158-0014
Edison P, 2021, Brain Connectivity and COVID-19, BRAIN CONNECTIVITY, Vol: 11, Pages: 251-252, ISSN: 2158-0014
Kobro-Flatmoen A, Lagartos-Donate MJ, Aman Y, et al., 2021, Re-emphasizing early Alzheimer's disease pathology starting in select entorhinal neurons, with a special focus on mitophagy, AGEING RESEARCH REVIEWS, Vol: 67, ISSN: 1568-1637
Edison P, 2021, Brain Connectivity and Alzheimer's Disease, BRAIN CONNECTIVITY, Vol: 11, Pages: 157-158, ISSN: 2158-0014
Edison P, 2021, Brain Connectivity and Alzheimer's Disease, Brain Connectivity, ISSN: 2158-0014
Edison P, Leng F, 2021, Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?, Nature Reviews Neurology, ISSN: 1759-4758
Edison P, 2021, Brain Connectivity: Neurocognitive Involvement in COVID-19, Brain Connectivity
Edison P, 2021, Brain Connectivity: Neurocognitive Involvement in COVID-19, BRAIN CONNECTIVITY, Vol: 11, Pages: 73-74, ISSN: 2158-0014
Leng F, Edison P, 2021, Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?, Nat Rev Neurol, Vol: 17, Pages: 157-172
Alzheimer disease (AD) is the most common form of neurodegenerative disease, estimated to contribute 60-70% of all cases of dementia worldwide. According to the prevailing amyloid cascade hypothesis, amyloid-β (Aβ) deposition in the brain is the initiating event in AD, although evidence is accumulating that this hypothesis is insufficient to explain many aspects of AD pathogenesis. The discovery of increased levels of inflammatory markers in patients with AD and the identification of AD risk genes associated with innate immune functions suggest that neuroinflammation has a prominent role in the pathogenesis of AD. In this Review, we discuss the interrelationships between neuroinflammation and amyloid and tau pathologies as well as the effect of neuroinflammation on the disease trajectory in AD. We specifically focus on microglia as major players in neuroinflammation and discuss the spatial and temporal variations in microglial phenotypes that are observed under different conditions. We also consider how these cells could be modulated as a therapeutic strategy for AD.
Edison P, Kobro-Flatmoen A, 2021, Re-emphasizing early Alzheimer's Disease pathology starting in select entorhinal neurons, with a special focus on mitophagy., Ageing Research Reviews, ISSN: 1568-1637
Femminella GD, Livingston NR, Raza S, et al., 2021, Does insulin resistance influence neurodegeneration in non-diabetic Alzheimer's subjects?, Alzheimers Research & Therapy, Vol: 13, Pages: 1-11, ISSN: 1758-9193
BackgroundType 2 diabetes is a risk factor for Alzheimer’s disease (AD), and AD brain shows impaired insulin signalling. The role of peripheral insulin resistance on AD aetiopathogenesis in non-diabetic patients is still debated. Here we evaluated the influence of insulin resistance on brain glucose metabolism, grey matter volume and white matter lesions (WMLs) in non-diabetic AD subjects.MethodsIn total, 130 non-diabetic AD subjects underwent MRI and [18F]FDG PET scans with arterial cannula insertion for radioactivity measurement. T1 Volumetric and FLAIR sequences were acquired on a 3-T MRI scanner. These subjects also had measurement of glucose and insulin levels after a 4-h fast on the same day of the scan. Insulin resistance was calculated by the updated homeostatic model assessment (HOMA2). For [18F]FDG analysis, cerebral glucose metabolic rate (rCMRGlc) parametric images were generated using spectral analysis with arterial plasma input function.ResultsIn this non-diabetic AD population, HOMA2 was negatively associated with hippocampal rCMRGlc, along with total grey matter volumes. No significant correlation was observed between HOMA2, hippocampal volume and WMLs.ConclusionsIn non-diabetic AD, peripheral insulin resistance is independently associated with reduced hippocampal glucose metabolism and with lower grey matter volume, suggesting that peripheral insulin resistance might influence AD pathology by its action on cerebral glucose metabolism and on neurodegeneration.
Edison P, 2021, Brain Connectivity: Advancing the Field of Neuroscience in the Era of COVID-19, Brain Connectivity, ISSN: 2158-0014
Edison P, 2021, Brain Connectivity: Advancing the Field of Neuroscience in the Era of COVID-19, BRAIN CONNECTIVITY, Vol: 11, Pages: 1-2, ISSN: 2158-0014
Femminella GD, Harold D, Scott J, et al., 2021, The Differential Influence of Immune, Endocytotic, and Lipid Metabolism Genes on Amyloid Deposition and Neurodegeneration in Subjects at Risk of Alzheimer’s Disease, Journal of Alzheimer's Disease, Vol: 79, Pages: 127-139, ISSN: 1387-2877
<jats:p>Background: Over 20 single-nucleotide polymorphisms (SNPs) are associated with increased risk of Alzheimer’s disease (AD). We categorized these loci into immunity, lipid metabolism, and endocytosis pathways, and associated the polygenic risk scores (PRS) calculated, with AD biomarkers in mild cognitive impairment (MCI) subjects. Objective: The aim of this study was to identify associations between pathway-specific PRS and AD biomarkers in patients with MCI and healthy controls. Methods: AD biomarkers ([18F]Florbetapir-PET SUVR, FDG-PET SUVR, hippocampal volume, CSF tau and amyloid-β levels) and neurocognitive tests scores were obtained in 258 healthy controls and 451 MCI subjects from the ADNI dataset at baseline and at 24-month follow up. Pathway-related (immunity, lipid metabolism, and endocytosis) and total polygenic risk scores were calculated from 20 SNPs. Multiple linear regression analysis was used to test predictive value of the polygenic risk scores over longitudinal biomarker and cognitive changes. Results: Higher immune risk score was associated with worse cognitive measures and reduced glucose metabolism. Higher lipid risk score was associated with increased amyloid deposition and cortical hypometabolism. Total, immune, and lipid scores were associated with significant changes in cognitive measures, amyloid deposition, and brain metabolism. Conclusion: Polygenic risk scores highlights the influence of specific genes on amyloid-dependent and independent pathways; and these pathways could be differentially influenced by lipid and immune scores respectively.</jats:p>
Leng F, Edison P, 2020, Neuroinflammation and microglial activation in Alzheimer’s disease: where do we go from here?, Nature Rev Neurol
Edison P, Maskery M, Gengler S, et al., 2020, The dual GLP-1/GIP receptor agonist DA4-JC shows superior protective properties in the APP/PS1 mouse model of Alzheimer's disease: Nonhuman?Lead optimization studies, Alzheimer's and Dementia, ISSN: 1552-5260
Edison P, Raza S, Femminella GD, et al., 2020, Relationship between spectral analysis, SUV and SUV Pons ratio as a measure of cerebral glucose metabolic rate in Alzheimer's Disease: Neuroimaging/multi-modal comparisons., Alzheimer's and Dementia, ISSN: 1552-5260
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