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Roy O. Weller

Researcher at Southampton General Hospital

Publications -  59
Citations -  4451

Roy O. Weller is an academic researcher from Southampton General Hospital. The author has contributed to research in topics: Cerebral amyloid angiopathy & Glymphatic system. The author has an hindex of 26, co-authored 59 publications receiving 3872 citations.

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Perivascular drainage of amyloid-beta peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease.

TL;DR: Therapeutic strategies that improve elimination of Abeta and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease.
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Ubiquitin-immunoreactive intraneuronal inclusions in amyotrophic lateral sclerosis. Morphology, distribution, and specificity.

TL;DR: It is concluded that the presence of ubiquitin-IR inclusions in lower motor neurons represents a characteristic pathological feature of ALS in its various clinical forms.
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Lymphatic Clearance of the Brain: Perivascular, Paravascular and Significance for Neurodegenerative Diseases.

TL;DR: The role of the vasculature and the impact of vascular pathology on the peri- and para-vascular clearance pathways of the brain are reviewed and the different views on the possible routes for ISF drainage of thebrain are discussed in the context of pathological significance.
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Perivascular drainage of solutes is impaired in the ageing mouse brain and in the presence of cerebral amyloid angiopathy

TL;DR: The hypothesis that perivascular solute drainage from the brain is altered both in the ageing brain and as a consequence of CAA is supported, which has implications for the success of therapeutic strategies for the treatment of AD that rely upon the health of the ageing cerebral vasculature.
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Consequence of Aβ immunization on the vasculature of human Alzheimer's disease brain

TL;DR: The findings are consistent with the hypothesis that Abeta immunization results in solubilization of plaque Abeta42 which, at least in part, exits the brain via the perivascular pathway, causing a transient increase in the severity of CAA.