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Antibodies against alpha-synuclein: tools and therapies
HBKU, Qatar Fdn, Neurol Disorder Res Ctr, QBRI, Doha, Qatar.
HBKU, Qatar Fdn, Neurol Disorder Res Ctr, QBRI, Doha, Qatar.
HBKU, Qatar Fdn, Neurol Disorder Res Ctr, QBRI, Doha, Qatar.
Newcastle Univ, Inst Neurosci, Campus Ageing & Vital, Newcastle Upon Tyne, Tyne & Wear, England.
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2019 (English)In: Journal of Neurochemistry, ISSN 0022-3042, E-ISSN 1471-4159, Vol. 150, no 5, p. 612-625Article, review/survey (Refereed) Published
Abstract [en]

Synucleinopathies including Parkinson's disease, dementia with Lewy bodies and multiple system atrophy are characterized by the abnormal accumulation and propagation of alpha-synuclein (alpha-syn) pathology in the central and peripheral nervous system as Lewy bodies or glial cytoplasmic inclusions. Several antibodies against alpha-syn have been developed since it was first detected as the major component of Lewy bodies and glial cytoplasmic inclusions. Over the years, researchers have generated specific antibodies that alleviate the accumulation of intracellular aggregated alpha-syn and associated pathology in cellular and preclinical models of synucleinopathies. So far, antibodies have been the first choice as tools for research and diagnosis and currently, a wide variety of antibody fragments have been developed as an alternative to full-length antibodies for increasing its therapeutic usefulness. Recently, conformation specific antibody-based approaches have been found to be promising as therapeutic strategies, both to block alpha-syn aggregation and ameliorate the resultant cytotoxicity, and as diagnostic tools. In this review, we summarize different alpha-syn specific antibodies and provide their usefulness in tackling synucleinopathies. 

Place, publisher, year, edition, pages
WILEY , 2019. Vol. 150, no 5, p. 612-625
Keywords [en]
antibodies, synucleinopathies, alpha-synuclein
National Category
Neurology Neurosciences
Identifiers
URN: urn:nbn:se:uu:diva-394144DOI: 10.1111/jnc.14713ISI: 000482407100012PubMedID: 31055836OAI: oai:DiVA.org:uu-394144DiVA, id: diva2:1357763
Available from: 2019-10-04 Created: 2019-10-04 Last updated: 2019-10-04Bibliographically approved

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Ingelsson, Martin

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