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Stuart M. Allan

Researcher at Manchester Academic Health Science Centre

Publications -  177
Citations -  12159

Stuart M. Allan is an academic researcher from Manchester Academic Health Science Centre. The author has contributed to research in topics: Stroke & Inflammation. The author has an hindex of 52, co-authored 156 publications receiving 10303 citations. Previous affiliations of Stuart M. Allan include University of Manchester & University of Glasgow.

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Cytokines and acute neurodegeneration

TL;DR: Evidence for the contribution of cytokines to acute neurodegeneration is reviewed, focusing primarily on interleukin 1, tumour necrosis factor-α (TNFα) and transforming growth factor-β (TGFβ).
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Interleukin-1 and neuronal injury

TL;DR: There is now extensive evidence to support the direct involvement of interleukin-1 in the neuronal injury that occurs in both acute and chronic neurodegenerative disorders, and a rationale for targeting the interleuko-1 system as a therapeutic strategy is provided.
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Vascular dysfunction-The disregarded partner of Alzheimer's disease

Melanie D. Sweeney, +71 more
TL;DR: Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize and should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.
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Impaired Adult Neurogenesis in the Dentate Gyrus of a Triple Transgenic Mouse Model of Alzheimer's Disease

TL;DR: 3xTg-AD mice have an impaired ability to generate new neurones in the DG of the hippocampus, the severity of which increases with age and might be directly associated with the known cognitive impairment observed from 6 months of age onwards.
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Systemic inflammatory stimulus potentiates the acute phase and CXC chemokine responses to experimental stroke and exacerbates brain damage via interleukin-1- and neutrophil-dependent mechanisms.

TL;DR: The data show for the first time that an acute systemic inflammatory stimulus is detrimental to outcome after experimental stroke and highlight IL-1 as a critical mediator in this paradigm, and suggestIL-1-induced potentiation of neutrophil mobilization via CXC chemokine induction is a putative mechanism underlying this effect.