A. M. Kennedy
Imperial College London
24 Papers
297 Citations
A. M. Kennedy is an academic researcher from Imperial College London. The author has contributed to research in topics: Alzheimer's disease & Dementia. The author has an hindex of 19, co-authored 24 publications. Previous affiliations of A. M. Kennedy include Hammersmith Hospital & University College Hospital.
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Papers
In-vivo measurement of activated microglia in dementia
Annachiara Cagnin,David J. Brooks,A. M. Kennedy,Roger N. Gunn,Ralph Myers,Federico Turkheimer,Terry Jones,Richard B. Banati,Richard B. Banati +8 more
TL;DR: In-vivo detection of increased [11C](R)-PK11195 binding in Alzheimer-type dementia, including mild and early forms, suggests that microglial activation is an early event in the pathogenesis of the disease.
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Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study.
Paul Edison,Hilary Archer,Alexander Gerhard,Alexander Gerhard,Rainer Hinz,Rainer Hinz,Nicola Pavese,Federico Turkheimer,Alexander Hammers,Yen F. Tai,Nick C. Fox,A. M. Kennedy,Martin N. Rossor,Martin N. Rossor,David J. Brooks,David J. Brooks +15 more
TL;DR: The inverse correlation between MMSE and microglial activation is compatible with a role of microglia in neuronal damage and the localisation of these increases to association areas is confirmed.
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Deficits in Cerebral Glucose Metabolism Demonstrated by Positron Emission Tomography in Individuals at Risk of Familial Alzheimer's Disease
A. M. Kennedy,Richard S. J. Frackowiak,Sarah K. Newman,P.M. Bloomfield,J. Seaward,P Roques,Graham Lewington,Vincent J. Cunningham,Martin N. Rossor +8 more
TL;DR: A significant reduction in global cerebral metabolic rate for glucose was found when compared with 16 age-matched controls and there was a focal, parieto-temporal deficit similar to, although less extensive than, that found in 18 symptomatic individuals from familial Alzheimer's disease (FAD) pedigrees.
261
Safety and efficacy of quinacrine in human prion disease (PRION-1 study): a patient-preference trial
John Collinge,John Collinge,Michele Gorham,Fleur Hudson,A. M. Kennedy,Geraldine Keogh,Geraldine Keogh,Suvankar Pal,Suvankar Pal,Martin N. Rossor,Peter Rudge,Durre Siddique,Durre Siddique,Moira Spyer,Dafydd Thomas,Dafydd Thomas,Sarah Walker,Tom R. Webb,Tom R. Webb,S Wroe,S Wroe,Janet Darbyshire +21 more
TL;DR: In this paper, the authors investigated the effect of quinacrine at a dose of 300 mg per day on the clinical course of human prion diseases in an open-label, patient-preference trial.
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Clinicopathological features of familial Alzheimer's disease associated with the M139V mutation in the presenilin 1 gene. Pedigree but not mutation specific age at onset provides evidence for a further genetic factor.
Nick C. Fox,A. M. Kennedy,Richard J. Harvey,Peter L. Lantos,P Roques,John Collinge,John Hardy,Michael Hutton,JM Stevens,Elizabeth K. Warrington,Martin N. Rossor +10 more
TL;DR: The pattern of cognitive decline was similar in both families: early memory loss was followed soon after by loss of arithmetic skills while naming and object perception skills were relatively preserved, and the diagnosis of Alzheimer's disease was confirmed with typical histopathology in one individual from each family.
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