Long-term effects of Abeta42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial.

By C. Holmes, D. Boche, D. Wilkinson, G. Yadegarfar, Vivienne Hopkins, A. Bayer, Roy W Jones, R. Bullock, S. Love, J. Neal and 2 more. The Lancet, 2008

1,443 citations recorded by the source corpus.

Subfields: Immunology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/08e069e9f584a9125571b66eb799997753fe6d98

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In Immunology

C. Cunningham

In Physiology

In Psychiatry and Mental health

Citations in the corpus

The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “…effect of amyloid immunization, it is also clear from the data from a limited number of cases, who have died after successful immunization (of events unrelated to treatment), that this approach will not give huge benefits at least when administered late in the disease (Holmes et al. 2008).”
A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “This activation is thought to result from the glial reaction to the events related to the ongoing deposition of Aβ [16–18].”
The Alzheimer’s Disease Neuroimaging Initiative: Progress report and future plans (2010, background): “A follow-up study of subjects in the Wyeth Elan 1792 vaccine trial showed amyloid removal (at pathology) in some subjects, while they continued to decline cognitively [9].”
Identification of Amyloid Plaques in Retinas from Alzheimer’s Patients and Noninvasive In Vivo Optical Imaging of Retinal Plaques in a Mouse Model (2010, neutral): “Therefore, there is a need for early diagnosis allowing early intervention, in order to achieve an efficient response to therapy (Holmes et al., 2008).”
White matter changes in Alzheimer’s disease: a focus on myelin and oligodendrocytes (2018, neutral): “Although there are toxic effects of Aβ on oligodendrocytes, clinical trials that have aimed to remove the Aβ plaque in symptomatic AD patients, did not prevent the progressive neurodegeneration and cognitive decline in AD patients [39, 72].”
Mechanisms of tau-induced neurodegeneration (2009, neutral): “modulating NSAID, Flurizan, as well as treatment with a drug (Alzhmed) that inhibits Ab aggregation, have all failed to show any significant clinical improvement in clinical trials on AD patients; (5) the clearance of b-amyloid plaques in the brains of patients with AD by Ab vaccine failed to reduce”
A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease (2010, background): “The pathophysiologic significance of the amyloid deposition on neuronal function is complex, as suggested by the observation of amyloid deposition in a significant number of cognitively healthy older subjects(12) and by postmortem studies in AD patients treated with amyloid immunization that show di”