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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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Presynaptic serotonergic dysfunction in patients with Alzheimer's disease.

TL;DR: Values for serotonergic markers in Alzheimer's disease samples did not show correlations with rating of the severity of dementia, indices of cholinergic innervation, or senile plaque and cortical pyramidal neurone loss, however, neuronbrillary tangle count and an index of glucose oxidation correlated with the concentration of 5‐hydroxyindoleacetic acid.
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The clinical diagnosis of early-onset dementias: diagnostic accuracy and clinicopathological relationships

TL;DR: Examination of subsyndromes of frontotemporal lobar degeneration showed a relatively predictable relationship between clinical diagnosis and pathological subtype, and showed that dementias can be distinguished in life with a high level of accuracy.
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Phenotypic variability associated with progranulin haploinsufficiency in patients with the common 1477C→T (Arg493X) mutation: an international initiative

TL;DR: Clinical heterogeneity is associated with GRN haploinsufficiency, and genetic variability on the wild-type GRN allele might have a role in the age-related disease penetrance of GRN mutations.
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Neuropsychological syndromes in presenile dementia due to cerebral atrophy.

TL;DR: The findings support the notion that the "cerebral atrophies" represent a heterogeneous group of conditions, and have relevance for the clinical diagnosis of presenile dementia.
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Evidence of Glutamatergic Denervation and Possible Abnormal Metabolism in Alzheimer's Disease

TL;DR: Early in the disease evidence of glutamatergic neurone loss is provided by the finding that in many regions of the cerebral cortex the Na+‐dependent uptake of D‐[3H]aspartic acid was almost always lowest in AD subjects compared with control when assessed by a method designed to minimise artifacts and epiphenomena.