Immunotherapy for Alzheimer's disease and other dementias
Immunotherapy for Alzheimer's disease and other dementias
Objective: The aim of this article is to review the role of immunotherapy in the removal of proteins which accumulate abnormally in neurodegenerative disorders associated with dementia, in particular amyloid-beta accumulation in Alzheimer's disease.
Results: In both transgenic mouse models and in two trials of amyloid-beta immunotherapy for human Alzheimer's disease, active immunization with amyloid-beta 1-42 results in the removal of amyloid-beta plaques from the cerebral cortex associated with, in the mouse models, improvement in cognitive function. Cerebral amyloid angiopathy and neurofibrillary tangles persist, however, and there is also concern about T lymphocyte immune reactions in the meninges in the human cases. Active immunization schedules are being developed to minimize T lymphocyte reactions and to maximize antibody production and passive immunization protocols are being devised. Immunotherapy for removal of the proteins which accumulate in other neurodegenerative disorders associated with dementia such as prion proteins and alpha-synuclein are in the early stages of development.
Conclusion: Dementias in the elderly are an increasing medical, social and economic problem and current treatments are only effective. In the majority of dementias, proteins accumulate within cells and in the extracellular compartments of the brain. In the most common dementia, Alzheimer's disease, amyloid-beta accumulates as plaques in the extracellular space of the grey matter and in artery walls as cerebral amyloid angiopathy and tau protein accumulates as neurofibrillary tangles within neurons
plaque removal, immunization, a-beta immunotherapy, prion, antibodies, pathogenesis, disease, prion disease, pathology, dementia, disorder, mouse model, trial, antibody, alzheimer's disease, cerebral amyloid angiopathy, immune-response, peptide, model, immunotherapy, treatment, disorders, interstitial fluid, neurodegenerative diseases
22-27
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
Nicoll, JAR.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Weller, RO.
4a501831-e38a-4d39-a125-d7141d6c667b
January 2006
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
Nicoll, JAR.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Weller, RO.
4a501831-e38a-4d39-a125-d7141d6c667b
Boche, D., Nicoll, JAR. and Weller, RO.
(2006)
Immunotherapy for Alzheimer's disease and other dementias.
Clinical Neuropharmacology, 29 (1), .
Abstract
Objective: The aim of this article is to review the role of immunotherapy in the removal of proteins which accumulate abnormally in neurodegenerative disorders associated with dementia, in particular amyloid-beta accumulation in Alzheimer's disease.
Results: In both transgenic mouse models and in two trials of amyloid-beta immunotherapy for human Alzheimer's disease, active immunization with amyloid-beta 1-42 results in the removal of amyloid-beta plaques from the cerebral cortex associated with, in the mouse models, improvement in cognitive function. Cerebral amyloid angiopathy and neurofibrillary tangles persist, however, and there is also concern about T lymphocyte immune reactions in the meninges in the human cases. Active immunization schedules are being developed to minimize T lymphocyte reactions and to maximize antibody production and passive immunization protocols are being devised. Immunotherapy for removal of the proteins which accumulate in other neurodegenerative disorders associated with dementia such as prion proteins and alpha-synuclein are in the early stages of development.
Conclusion: Dementias in the elderly are an increasing medical, social and economic problem and current treatments are only effective. In the majority of dementias, proteins accumulate within cells and in the extracellular compartments of the brain. In the most common dementia, Alzheimer's disease, amyloid-beta accumulates as plaques in the extracellular space of the grey matter and in artery walls as cerebral amyloid angiopathy and tau protein accumulates as neurofibrillary tangles within neurons
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Published date: January 2006
Additional Information:
(Reprinted from Curr. Opin. Neurol. vol 118, 720-725, 2005)
Keywords:
plaque removal, immunization, a-beta immunotherapy, prion, antibodies, pathogenesis, disease, prion disease, pathology, dementia, disorder, mouse model, trial, antibody, alzheimer's disease, cerebral amyloid angiopathy, immune-response, peptide, model, immunotherapy, treatment, disorders, interstitial fluid, neurodegenerative diseases
Identifiers
Local EPrints ID: 62329
URI: http://eprints.soton.ac.uk/id/eprint/62329
ISSN: 0362-5664
PURE UUID: 81b8c7d4-f6fb-494b-8b05-0dd249be76aa
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Date deposited: 18 Sep 2008
Last modified: 23 Jul 2022 01:50
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Author:
RO. Weller
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