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Long-term effects of Aβ42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial
Abstract
Background Immunisation of patients with Alzheimer's disease with full-length amyloid-beta peptide (Abeta(42)) can clear amyloid plaques from the brain. Our aim was to assess the relation between Abeta(42) immune response, degree of plaque removal, and long-term clinical outcomes.Methods In June, 2003, consent for long-term clinical follow-up, post-mortem neuropathological examination, or both, was sought from 80 patients (or their carers) who had entered a phase I randomised, placebo-controlled trial of immunisation with Abeta(42) (AN1792, Elan Pharmaceuticals) in September, 2000. The follow-up study was completed in September, 2006. Plaques were assessed in terms of the percentage area of the cortex with Abeta immunostaining (Abeta load) and in terms of characteristic histological features reflecting plaque removal. Survival of all 80 individuals until severe dementia or death was assessed with a Cox proportional hazard model.Findings 20 participants--15 in the AN1792 group, five in the placebo group--died before follow-up started. A further 22 patients--19 in the AN1792 group, three in the placebo group--died during follow-up. Nine of the deceased patients, all in the AN1792 group, had given consent for post-mortem analysis; one of these who did not die with Alzheimer's disease was excluded. In the remaining eight participants who received immunisation and who were examined neuropathologically, mean Abeta load was lower than in an unimmunised control group that was matched for age at death (2.1% [SE 0.7] in treated participants vs 5.1% [0.9] in controls; mean difference 3.0%, 95% CI 0.6-5.4; p=0.02). Although there was considerable variation in Abeta load and degree of plaque removal among immunised participants, the degree of plaque removal varied significantly with mean antibody response attained during the treatment study period (Kruskal-Wallis p=0.02). Seven of the eight immunised patients who underwent post-mortem assessment, including those with virtually complete plaque removal, had severe end stage dementia before death. In the whole cohort, there was no evidence of improved survival (hazard ratio 0.93, 95% CI 0.43-3.11; p=0.86) or of an improvement in the time to severe dementia (1.18, 0.45-3.11; p=0.73) in the AN1792 group versus the placebo group.Interpretation Although immunisation with Abeta(42) resulted in clearance of amyloid plaques in patients with Alzheimer's disease, this clearance did not prevent progressive neurodegeneration.
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“A study involving cognitively healthy adults showed that Aβ in CSF or the hippocampus increases after sleep deprivation or slow-wave sleep disruption, which indicates the complexity of Aβ kinetics [59, 60, 61].”
From Clinical trials of new drugs for Alzheimer disease (2020) · cites this paper as [61]
In the citing paper
“Several anti-Aβ therapeutic strategies are being pursued to treat AD; however, it is likely that treatment will need to begin during the preclinical phase to prevent or limit plaque accumulation to be beneficial in reducing the risk of developing AD (51, 52).”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [51]
In the citing paper
“Recent clinical trials attempting to replicate the benefits of Aβ immunotherapy seen in mouse models have been primarily unsuccessful in preventing early cognitive decline in AD patients despite significantly decreasing the amyloid burden”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Holmes et al., 2008
In the citing paper
“While safety concerns caused this trial to terminate prematurely, subsequent clinical analyses were at best unimpressive [250, 251].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [251]
In the citing paper
“There have been cases in which individuals with mid- to late-stage clinical AD were administered anti-Aβ immunotherapy that partially cleared AβPs, but this clearance did not seem to mitigate NFT formation or the inexorable disease course (69-71).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [70]
In the citing paper
“Often neglected is the question of lesion turnover (i.e. AβPs being possibly reabsorbed during life so that they would not be “counted” at autopsy), which seems to occur in some subjects (70, 270).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [70]
In the citing paper
“Aβ vaccine trials also attest to the ability of the immune system to clear diffuse AβPs (69, 70, 271), but it is not known whether toxic APP metabolites or other plaque components remain after clearance of fibrillar Aβ-peptides (73, 272).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [70]
In the citing paper
“a subset of patients from the aborted Wyeth/ELAN active Aβ vaccine trial that were studied at autopsy showed Aβ plaque removal in the absence of cognitive improvement [75].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [75]
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Ross, J., & Imbimbo, B. P. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-101548 · Cited by 8
Cognitive Function in Health and Disease: The Role of Epigenetic Mechanisms
Mungenast, A. E., & Tsai, L. (2012) · Neurodegenerative Diseases · doi:10.1159/000334602 · Cited by 9
Pro: Can neuropathology really confirm the exact diagnosis?
Esiri, M. M. (2010) · Alzheimer s Research & Therapy · doi:10.1186/alzrt33 · Cited by 7
Davtyan, H., Ghochikyan, A., Hovakimyan, A., Petrushina, I., Yu, J., Flyer, D. C., Madsen, P. J., Pedersen, L. Ø., Cribbs, D. H., & Agadjanyan, M. G. (2014) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2014.01.002 · Cited by 9
“Data from preclinical studies (Petrushina et al., 2007) as well as from the first clinical trial AN1792 (Patton et al., 2006; Holmes et al., 2008) argue that high titers of long lasting anti-Aβ antibody could be beneficial in reduction of Aβ-deposits in the brain and in improvement of cognitive…”
Macklin, E. A., Blacker, D., Hyman, B. T., & Betensky, R. A. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-122212 · Cited by 8
Alzheimer’s Disease – The Importance of Early Detection
Todd, S., & Passmore, P. (2008) · European Neurological Review · doi:10.17925/enr.2008.03.02.18 · Cited by 8
Immunotherapies Targeting α -Synuclein in Parkinson Disease
Jamal, F. (2020) · Federal Practitioner · doi:10.12788/fp.0026 · Cited by 10
Alzheimer’s Disease: Current and Future Treatments. A Review
Chou, E. (2014) · International Journal of Medical Students · doi:10.5195/ijms.2014.85 · Cited by 8
“On top of this, some patients even progressed to clinically severe dementia.(55) What these results imply is that the removal of NPs alone may be insufficient in the disease-modifying treatment of AD.”
Les nouveaux critères de la Maladie d’Alzheimer – Perspective gériatrique*
Molin, P., & Rockwood, K. J. (2016) · Canadian Geriatrics Journal · doi:10.5770/cgj.19.242 · Cited by 13
“Par exemple, il a été suggéré que l’exigence d’un biomarqueur témoignant du dépôt d’Aβ cérébrale pour le recrutement de sujets n’améliore pas l’efficacité des essais cliniques(17) et que l’élimination de la pathologie ne réduit pas la survenue de démence(18).”
Checler, F., & Buée, L. (2009) · Annales Pharmaceutiques Françaises · doi:10.1016/j.pharma.2009.01.002 · Cited by 12
Feasibility of Predicting MCI/AD Using Neuropsychological Tests and Serum β‐Amyloid
Luis, C. A., Abdullah, L. I., Ait‐Ghezala, G., Mouzon, B., Keegan, A. P., Crawford, F., & MULLAN, M. J. (2011) · International Journal of Alzheimer s Disease · doi:10.4061/2011/786264 · Cited by 8
Ritchie, C. W., Masters, C. L., Mason, S., Li, Q., & McShane, R. H. (2011) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd008782.pub3 · Cited by 7
Many are called, yet few are chosen. Are neuropsychiatric clinical trials letting us down?
McArthur, R. A. (2010) · Drug Discovery Today · doi:10.1016/j.drudis.2010.12.005 · Cited by 8
Afrakoti, L. G. M. P., Moghadam, S. D., & Hadinezhad, P. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251329188 · Cited by 12
“214 The application of crenezumab in mild-to-moderate AD cases in phase II like gantenerumab application in prodromal AD patients in a phase III trial 245 did not yield clinical effectiveness in improving the cognition scores.”
InfluentialA century of confusion in researching Alzheimer’s disease
Garrett, M. D., & Valle, R. (2016) · International Journal of Healthcare · doi:10.5430/ijh.v2n2p13 · Cited by 7
Dissecting the immune response of CD4+ T cells in Alzheimer’s disease
Kostić, M. S., Živković, N., Cvetanović, A., Bašić, J., & Stojanović, I. R. (2024) · Reviews in the Neurosciences · doi:10.1515/revneuro-2024-0090 · Cited by 8
Caselli, R. J. (2012) · Alzheimer s Research & Therapy · doi:10.1186/alzrt123 · Cited by 7
Holtzman, J. L. (2013) · Frontiers in Pharmacology · doi:10.3389/fphar.2013.00059 · Cited by 7
Clinical issues in old age ‐ the challenges of geriatric medicine
Bayer, A. J. (2011) · Quality in Ageing and Older Adults · doi:10.5042/qiaoa.2011.0145 · Cited by 7
Self-citationPharmacological Treatment of Alzheimer’s Disease
Schneider, L. S. (2012) · Advances in biological psychiatry · doi:10.1159/000335407 · Cited by 7
Cunningham, E. L., & Passmore, A. P. (2013) · Maturitas · doi:10.1016/j.maturitas.2013.04.013 · Cited by 7
Beyond diagnosis: What biomarkers are teaching us about the “bio”logy of Alzheimer disease
Rabinovici, G. D., & Roberson, E. D. (2010) · Annals of Neurology · doi:10.1002/ana.22020 · Cited by 7
“Do plaques in these individuals represent a benign accompaniment to normal aging, or are they indicative of preclinical disease? Resolving this fundamental question about the relationship between A and AD has become even more pressing in light of disappointing results from clinical trials of A -directed therapies,(5,6…”
Result
Metadata
- Authors
- Holmes, C., Boche, D., Wilkinson, D., Yadegarfar, G., Hopkins, V., Bayer, A., Jones, R. W., Bullock, R., Love, S., Neal, J. W., Zotova, E., & Nicoll, J. A.
- Affiliations
- Moorgreen Hospital (GB)
- University of Southampton (GB)
- Isfahan University of Medical Sciences (IR)
- Royal United Hospital (GB)
- University of Bristol (GB)
- University of Wales (GB)
- University Hospital Southampton NHS Foundation Trust (GB)
- ORCID
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2008-07
- Volume
- 372
- Issue
- 9634
- Pages
- 216-223
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2152446053
- Semantic Scholar
- 08e069e9f584a9125571b66eb799997753fe6d98
- Cited by
- 1,416
- References
- 33
- Citations by year
- 2026: 18 · 2025: 26 · 2024: 30 · 2023: 34 · 2022: 46 · 2021: 52 · 2020: 58 · 2019: 61 · 2018: 58 · 2017: 73 · 2016: 71 · 2015: 82 · 2014: 113 · 2013: 115 · 2012: 120
- FWCI
- 102.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- University of Oxford
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid plaques, dental plaque removal, amyloid load, long-term clinical outcomes, survival, dementia progression, postmortem neuropathology, immunotherapy safety and efficacy, autopsy
- MeSH terms
- Aged, Alzheimer Disease, Antibody Formation, Follow-Up Studies, Humans, Randomized Controlled Trials as Topic, Amyloid beta-Peptides, Clinical Trials, Phase I as Topic, Plaque, Amyloid
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