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David Neary

Researcher at Salford Royal NHS Foundation Trust

Publications -  220
Citations -  33304

David Neary is an academic researcher from Salford Royal NHS Foundation Trust. The author has contributed to research in topics: Frontotemporal dementia & Dementia. The author has an hindex of 78, co-authored 206 publications receiving 31481 citations. Previous affiliations of David Neary include University of Salford & Manchester Academic Health Science Centre.

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Sensitivity and specificity of FTDC criteria for behavioral variant frontotemporal dementia

TL;DR: Revised diagnostic criteria for behavioral variant frontotemporal dementia show encouragingly high sensitivity and specificity when applied to patients with early-onset dementia and provide a useful tool both for specialist researchers and general clinicians.
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Monoamine metabolite concentrations in lumbar cerebrospinal fluid of patients with histologically verified Alzheimer's dementia.

TL;DR: CSF HVA increased with age in control but not in Alzheimer patients, and HVA and 5-HIAA in the CSF of presenile Alzheimer patients was lower than that of age matched control subjects.
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Cholinesterase activities in cerebrospinal fluid of patients with senile dementia of Alzheimer type.

TL;DR: A molecular defect in the AChE in the ventricular CSF of Alzheimer patients is indicated by the finding that the enzyme failed to show inhibition by high concentrations of substrate, which may form the basis for a diagnostic test of Alzheimer type dementia.
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The electroencephalogram in dementia with Lewy bodies

TL;DR: It is suggested that although patients with DLB have a more aggressive course than AD, EEG abnormalities do not differ in the 2 groups, and it is believed the EEG provides important supporting diagnostic information in DLB.
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Imbalance of a serotonergic system in frontotemporal dementia: implication for pharmacotherapy

TL;DR: Neurochemical results in FTD indicate degeneration and loss of pyramidal neurones in frontotemporal neocortex, yet 5-HT afferents and5-HT concentration, which are inhibitory on pyramid neurones, were relatively preserved, which could lead to an excess of extraneural 5- HT causing underactivity of surviving pyramides.