Imperial College London

Professor Paul Edison

Faculty of MedicineDepartment of Brain Sciences

Professor of Neuroscience
 
 
 
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Contact

 

paul.edison

 
 
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Location

 

2S 5A, Level 2Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

230 results found

Hönig M, Altomare D, Caprioglio C, Collij L, Barkhof F, Van Berckel B, Scheltens P, Farrar G, Battle MR, Theis H, Giehl K, Bischof GN, Garibotto V, Molinuevo JLL, Grau-Rivera O, Delrieu J, Payoux P, Demonet JF, Nordberg AK, Savitcheva I, Walker Z, Edison P, Stephens AW, Gismondi R, Jessen F, Buckley CJ, Gispert JD, Frisoni GB, Drzezga A, AMYPAD Consortiumet al., 2024, Association Between Years of Education and Amyloid Burden in Patients With Subjective Cognitive Decline, MCI, and Alzheimer Disease., Neurology, Vol: 102

OBJECTIVES: Higher-educated patients with Alzheimer disease (AD) can harbor greater neuropathologic burden than those with less education despite similar symptom severity. In this study, we assessed whether this observation is also present in potential preclinical AD stages, namely in individuals with subjective cognitive decline and clinical features increasing AD likelihood (SCD+). METHODS: Amyloid-PET information ([18F]Flutemetamol or [18F]Florbetaben) of individuals with SCD+, mild cognitive impairment (MCI), and AD were retrieved from the AMYPAD-DPMS cohort, a multicenter randomized controlled study. Group classification was based on the recommendations by the SCD-I and NIA-AA working groups. Amyloid PET images were acquired within 8 months after initial screening and processed with AMYPYPE. Amyloid load was based on global Centiloid (CL) values. Educational level was indexed by formal schooling and subsequent higher education in years. Using linear regression analysis, the main effect of education on CL values was tested across the entire cohort, followed by the assessment of an education-by-diagnostic-group interaction (covariates: age, sex, and recruiting memory clinic). To account for influences of non-AD pathology and comorbidities concerning the tested amyloid-education association, we compared white matter hyperintensity (WMH) severity, cardiovascular events, depression, and anxiety history between lower-educated and higher-educated groups within each diagnostic category using the Fisher exact test or χ2 test. Education groups were defined using a median split on education (Md = 13 years) in a subsample of the initial cohort, for whom this information was available. RESULTS: Across the cohort of 212 individuals with SCD+ (M(Age) = 69.17 years, F 42.45%), 258 individuals with MCI (M(Age) = 72.93, F 43.80%), and 195 individuals with dementia (M(Age) = 74.07, F 48.72%), no main effect of education (ß = 0.52, 95% CI -0.30 to 1.58), but a significan

Journal article

Edison P, 2024, Astroglial activation: Current concepts and future directions., Alzheimers Dement

Astrocytes are abundantly and ubiquitously expressed cell types with diverse functions throughout the central nervous system. Astrocytes show remarkable plasticity and exhibit morphological, molecular, and functional remodeling in response to injury, disease, or infection of the central nervous system, as evident in neurodegenerative diseases. Astroglial mediated inflammation plays a prominent role in the pathogenesis of neurodegenerative diseases. This review focus on the role of astrocytes as essential players in neuroinflammation and discuss their morphological and functional heterogeneity in the normal central nervous system and explore the spatial and temporal variations in astroglial phenotypes observed under different disease conditions. This review discusses the intimate relationship of astrocytes to pathological hallmarks of neurodegenerative diseases. Finally, this review considers the putative therapeutic strategies that can be deployed to modulate the astroglial functions in neurodegenerative diseases. HIGHLIGHTS: Astroglia mediated neuroinflammation plays a key role in the pathogenesis of neurodegenerative diseases. Activated astrocytes exhibit diverse phenotypes in a region-specific manner in brain and interact with β-amyloid, tau, and α-synuclein species as well as with microglia and neuronal circuits. Activated astrocytes are likely to influence the trajectory of disease progression of neurodegenerative diseases, as determined by the stage of disease, individual susceptibility, and state of astroglial priming. Modulation of astroglial activation may be a therapeutic strategy at various stages in the trajectory of neurodegenerative diseases to modify the disease course.

Journal article

Patel V, Edison P, 2024, Cardiometabolic risk factors and neurodegeneration: a review of the mechanisms underlying diabetes, obesity and hypertension in Alzheimer's disease., J Neurol Neurosurg Psychiatry

A growing body of evidence suggests that cardiometabolic risk factors play a significant role in Alzheimer's disease (AD). Diabetes, obesity and hypertension are highly prevalent and can accelerate neurodegeneration and perpetuate the burden of AD. Insulin resistance and enzymes including insulin degrading enzymes are implicated in AD where breakdown of insulin is prioritised over amyloid-β. Leptin resistance and inflammation demonstrated by higher plasma and central nervous system levels of interleukin-6 (IL-6), IL-1β and tumour necrosis factor-α, are mechanisms connecting obesity and diabetes with AD. Leptin has been shown to ameliorate AD pathology and enhance long-term potentiation and hippocampal-dependent cognitive function. The renin-aldosterone angiotensin system, involved in hypertension, has been associated with AD pathology and neurotoxic reactive oxygen species, where angiotensin binds to specific angiotensin-1 receptors in the hippocampus and cerebral cortex. This review aims to consolidate the evidence behind putative processes stimulated by obesity, diabetes and hypertension, which leads to increased AD risk. We focus on how novel knowledge can be applied clinically to facilitate recognition of efficacious treatment strategies for AD.

Journal article

Nowell J, Blunt E, Gupta D, Edison Pet al., 2023, Antidiabetic agents as a novel treatment for Alzheimer's and Parkinson's disease, AGEING RESEARCH REVIEWS, Vol: 89, ISSN: 1568-1637

Journal article

Edison P, 2023, Brain Connectivity: <i>A Journal of Clinical Neurology, Neuroscience, & Neuroimaging</i> Advancing the Field of Neurology, BRAIN CONNECTIVITY, Vol: 13, Pages: 265-265, ISSN: 2158-0014

Journal article

Lo Re V, Avorio F, Russelli G, Bulati M, Panarello G, Edison P, De Erausquin Get al., 2023, Neurological manifestations of SARSCoV-2 infection in solid organ transplant: a single centre retrospective study, Publisher: WILEY, Pages: 295-295, ISSN: 1351-5101

Conference paper

Altomare D, Barkhof F, Caprioglio C, Collij LE, Scheltens P, Lopes Alves I, Bouwman F, Berkhof J, van Maurik IS, Garibotto V, Moro C, Delrieu J, Payoux P, Saint-Aubert L, Hitzel A, Molinuevo JL, Grau-Rivera O, Gispert JD, Drzezga A, Jessen F, Zeyen P, Nordberg A, Savitcheva I, Jelic V, Walker Z, Edison P, Demonet J-F, Gismondi R, Farrar G, Stephens AW, Frisoni GBet al., 2023, Clinical Effect of Early vs Late Amyloid Positron Emission Tomography in Memory Clinic Patients The AMYPAD-DPMS Randomized Clinical Trial, JAMA NEUROLOGY, Vol: 80, Pages: 548-557, ISSN: 2168-6149

Journal article

Crook H, Ramirez A, Hosseini A, Vavougyios G, Lehmann C, Bruchfeld J, Schneider A, D'Avossa G, Lo Re V, Salmoiraghi A, Mukaetova-Ladinska E, Katshu M, Boneschi FM, Hakansson K, Geerlings M, Pracht E, Ruiz A, Jansen JFA, Snyder H, Kivipelto M, Edison Pet al., 2023, European Working Group on SARS-CoV-2: Current Understanding, Unknowns, and Recommendations on the Neurological Complications of COVID-19, BRAIN CONNECTIVITY, Vol: 13, Pages: 178-210, ISSN: 2158-0014

Journal article

Edison P, 2023, Brain Connectivity: A Journal of Clinical Neurology, Neuroscience, & Neuroimaging Advancing the Field of Neurology, BRAIN CONNECTIVITY, Vol: 13, Pages: 175-177, ISSN: 2158-0014

Journal article

Edison P, 2023, Brain Connectivity: A Journal of Clinical Neurology, Neuroscience, & Neuroimaging Advancing the Field of Neurology, BRAIN CONNECTIVITY, Vol: 13, Pages: 117-119, ISSN: 2158-0014

Journal article

Fleming B, Edison P, Kenny L, 2023, Cognitive impairment after cancer treatment: mechanisms, clinical characterization, and management, BMJ-BRITISH MEDICAL JOURNAL, Vol: 380, ISSN: 0959-535X

Journal article

Leng F, Hinz R, Gentleman S, Hampshire A, Dani M, Brooks DJ, Edison Pet al., 2023, Neuroinflammation is independently associated with brain network dysfunction in Alzheimer's disease, MOLECULAR PSYCHIATRY, Vol: 28, Pages: 1303-1311, ISSN: 1359-4184

Journal article

Edison P, 2023, <i>Brain Connectivity: A Journal of Clinical Neurology, Neuroscience, & Neuroimaging</i> Advancing the Field of Neurology, BRAIN CONNECTIVITY, Vol: 13, Pages: 1-3, ISSN: 2158-0014

Journal article

Caprioglio C, Ribaldi F, Visser LNC, Minguillon C, Collij LE, Grau-Rivera O, Zeyen P, Molinuevo JL, Domingo Gispert J, Garibotto V, Moro C, Walker Z, Edison P, Demonet J-F, Barkhof F, Scheltens P, Alves IL, Gismondi R, Farrar G, Stephens AW, Jessen F, Frisoni GB, Altomare Det al., 2023, Analysis of Psychological Symptoms Following Disclosure of Amyloid-Positron Emission Tomography Imaging Results to Adults With Subjective Cognitive Decline, JAMA NETWORK OPEN, Vol: 6, ISSN: 2574-3805

Journal article

Nowell J, Blunt E, Edison P, 2023, Incretin and insulin signaling as novel therapeutic targets for Alzheimer's and Parkinson's disease, MOLECULAR PSYCHIATRY, Vol: 28, Pages: 217-229, ISSN: 1359-4184

Journal article

Edison P, 2022, Brain Connectivity: A Journal of Clinical Neurology, Neuroscience, & Neuroimaging Advancing the Field of Neurology, BRAIN CONNECTIVITY, Vol: 12, Pages: 847-849, ISSN: 2158-0014

Journal article

Pasqualetti G, Thayanandan T, Edison P, 2022, Influence of genetic and cardiometabolic risk factors in Alzheimer?s disease, AGEING RESEARCH REVIEWS, Vol: 81, ISSN: 1568-1637

Journal article

Mohamed MA, Zeng Z, Gennaro M, Lao-Kaim N, Myers J, Calsolaro V, Femminella G, Tyacke R, Martin-Bastida A, Gunn R, Nutt D, Edison P, Piccini P, Roussakis Aet al., 2022, Astrogliosis in aging and Parkinson’s disease dementia: a new clinical study with 11C-BU99008 PET, Brain Communications, Vol: 4, ISSN: 2632-1297

The role of astrogliosis in the pathology of brain aging and neurodegenerative diseases has recently drawn great attention. Imidazoline-2 binding sites (I2BS) represent a possible target to map the distribution of reactive astrocytes. In this study, we use 11C-BU99008, an I2BS-specific PET radioligand, to image reactive astrocytes in vivo in healthy controls (HCs) andpatients with established Parkinson’s disease dementia (PDD).Eighteen HCs (age: 45−78 years) and six patients with PDD (age: 64−77 years) had one 11C-BU99008 PET-CT scan with arterial input function. All subjects underwent one 3T MRI brain scan to facilitate the analysis of the PET-CT data and to capture individual cerebral atrophy. Regional 11C-BU99008 volumes of distribution (VT) were calculated for each subject by two-tissue compartmental modelling.Positive correlations between 11C-BU99008 VT values and age were found for all tested regions across the brain within HCs (p<0.05); furthermore, multiple regression indicated that aging affects 11C-BU99008 VT values in a region-specific manner. Independent samples t-test indicated that there was no significant group difference in 11C-BU99008 VT values betweenPDD (n=6; mean age = 71.97±4.66 years) and older HCs (n=9; mean age = 71.90±5.51 years).Our dataset shows that astrogliosis is common with aging in a region-specific manner. However, in this set-up, 11C-BU99008 PET cannot differentiate patients with PDD from healthy controls of similar age.

Journal article

Edison P, 2022, Brain Connectivity: A Journal of Clinical Neurology, Neuroscience, and Neuroimaging, BRAIN CONNECTIVITY, Vol: 12, Pages: 498-501, ISSN: 2158-0014

Journal article

Loreto F, Fitzgerald A, Golemme M, Gunning S, Win Z, Patel N, Carswell C, Perry R, Kennedy A, Edison P, Malhotra Pet al., 2022, Prevalence of depressive symptoms in a memory clinic cohort: a retrospective study, Journal of Alzheimer's Disease, Vol: 88, ISSN: 1387-2877

Background Depression has been suggested to be a cause of reversible cognitive impairment but also a risk factor for neurodegenerative disease. Studies suggest that depression prevalence may be high in early onset dementia, particularly Alzheimer’s disease, but this has not been systematically assessed in a biomarker-validated clinical dementia cohort to date. Objective To examine the prevalence, features and association with amyloid pathology of lifetime depressive symptoms in a memory clinic cohort meeting appropriate use criteria for amyloid PET imaging.Methods We included 300 patients from a single-centre memory clinic cohort that received diagnostic biomarker evaluation with amyloid PET imaging according to appropriate use criteria. History of lifetime depressive symptoms was retrospectively assessed through structured review of clinical correspondence. Results One-hundred-and-forty-two (47%) patients had a history of significant depressive symptoms (‘D+’). Of these, 89% had ongoing symptoms and 60% were on antidepressants at the time of presentation to our Clinic. Depressive symptoms were equally highly prevalent in the amyloid-positive and the heterogeneous group of amyloid-negative patients.Conclusions Approximately half of patients who meet appropriate use criteria for amyloid PET had a history of depressive symptoms. We suggest that depression is an important feature of both neurodegenerative and non-neurodegenerative cognitive impairment and may contribute to the diagnostic uncertainty behind referral to amyloid PET.

Journal article

Edison P, 2022, <i>Brain Connectivity???????</i>: A Journal of Clinical Neurology and Neuroscience, BRAIN CONNECTIVITY, Vol: 12, Pages: 299-301, ISSN: 2158-0014

Journal article

Young M, Crook H, Scott J, Edison Pet al., 2022, Covid-19: virology, variants, and vaccines, BMJ Medicine, Vol: 1, ISSN: 2754-0413

As of 25 January 2022, over 349 million individuals have received a confirmed diagnosis of covid-19, with over 5.59 million confirmed deaths associated with the SARS-CoV-2 virus. The covid-19 pandemic has prompted an extensive global effort to study the molecular evolution of the virus and develop vaccines to prevent its spread. Although rigorous determination of SARS-CoV-2 infectivity remains elusive, owing to the continuous evolution of the virus, steps have been made to understand its genome, structure, and emerging genetic mutations. The SARS-CoV-2 genome is composed of several open reading frames and structural proteins, including the spike protein, which is essential for entry into host cells. As of 25 January 2022, the World Health Organization has reported five variants of concern, two variants of interest, and three variants under monitoring. Additional sublineages have since been identified, and are being monitored. The mutations harboured in these variants confer an increased transmissibility, severity of disease, and escape from neutralising antibodies compared with the primary strain. The current vaccine strategy, including booster doses, provides protection from severe disease. As of 24 January 2022, 33 vaccines have been approved for use in 197 countries. In this review, we discuss the genetics, structure, and transmission methods of SARS-CoV-2 and its variants, highlighting how mutations provide enhanced abilities to spread and inflict disease. This review also outlines the vaccines currently in use around the world, providing evidence for every vaccine's immunogenicity and effectiveness.

Journal article

Edison P, 2022, <i>Brain Connectivity:</i> A Clinical Neurology and Neuroscience Journal, BRAIN CONNECTIVITY, Vol: 12, Pages: 207-209, ISSN: 2158-0014

Journal article

Livingston NR, Calsolaro V, Hinz R, Nowell J, Raza S, Gentleman S, Tyacke RJ, Myers J, Venkataraman AV, Perneczky R, Gunn RN, Rabiner EA, Parker CA, Murphy PS, Wren PB, Nutt DJ, Matthews PM, Edison Pet al., 2022, Relationship between astrocyte reactivity, using novel <SUP>11</SUP>C-BU99008 PET, and glucose metabolism, grey matter volume and amyloid load in cognitively impaired individuals, MOLECULAR PSYCHIATRY, Vol: 27, Pages: 2019-2029, ISSN: 1359-4184

Journal article

Edison P, 2022, <i>Brain Connectivity</i>: A Journal of Clinical Neurology and Neuroscience, BRAIN CONNECTIVITY, Vol: 12, Pages: 109-111, ISSN: 2158-0014

Journal article

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