Cited by 348Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Mass spectrometric characterization of brain amyloid beta isoform signatures in familial and sporadic Alzheimer’s disease

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Portelius, Erik, Bogdanovic, Nenad, Gustavsson, Mikael K., Volkmann, Inga, Brinkmalm, Gunnar, Zetterberg, Henrik, Winblad, Bengt, Blennow, Kaj·2010·Acta Neuropathologica

DOI 10.1007/s00401-010-0690-1PMC PMC3568930

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Abstract

A proposed key event in the pathogenesis of Alzheimer's disease (AD) is the formation of neurotoxic amyloid beta (Abeta) oligomers and amyloid plaques in specific brain regions that are affected by the disease. The main plaque component is the 42 amino acid isoform of Alphabeta (Abeta1-42), which is thought to initiate plaque formation and AD pathogenesis. Numerous isoforms of Abeta, e.g., Abeta1-42, Abeta1-40 and the 3-pyroglutamate derivate of Abeta3-42 (pGluAbeta3-42), have been detected in the brains of sporadic AD (SAD) and familial AD (FAD) subjects. However, the relative importance of these isoforms in the pathogenesis of AD is not fully understood. Here, we report a detailed study using immunoprecipitation in combination with mass spectrometric analysis to determine the Abeta isoform pattern in the cerebellum, cortex and hippocampus in AD, including subjects with a mutation in the presenilin (M146V) or amyloid precursor protein (KM670/671NL) genes, SAD subjects and non-demented controls. We show that the dominating Abeta isoforms in the three different brain regions analyzed from control, SAD, and FAD are Abeta1-42, pGluAbeta3-42, Abeta4-42 and Abeta1-40 of which Abeta1-42 and Abeta4-42 are the dominant isoforms in the hippocampus and the cortex in all groups analyzed, controls included. No prominent differences in Abeta isoform patterns between FAD and SAD patients were seen, underscoring the similarity in the amyloid pathology of these two disease entities.

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Authors: Portelius, E., Bogdanovic, N., Gustavsson, M. K., Volkmann, I., Brinkmalm, G., Zetterberg, H., Winblad, B., & Blennow, K.
Affiliations: University of Gothenburg (SE)
Karolinska Institutet (SE)
Corresponding author: Portelius, Erik
ORCID: Portelius, Erik
Brinkmalm, Gunnar
Zetterberg, Henrik
Winblad, Bengt
Blennow, Kaj
Venue: Acta Neuropathologica
Publisher: Springer Science and Business Media LLC
Published: 2010-04-24
Volume: 120
Issue: 2
Pages: 185-193
ISSN: 0001-6322 (ISSN-L)
1432-0533
DOI: 10.1007/s00401-010-0690-1
PMC: PMC3568930
OpenAlex: W2045197448
Cited by: 348
References: 41
Citations by year: 2026: 13 · 2025: 19 · 2024: 27 · 2023: 22 · 2022: 21 · 2021: 25 · 2020: 26 · 2019: 28 · 2018: 26 · 2017: 20 · 2016: 22 · 2015: 31 · 2014: 23 · 2013: 10 · 2012: 16
FWCI: 9.75
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Acta Neuropathologica (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
UCL Discovery (University College London) (submittedVersion)
Funders: National Institute on Aging (K08 AG-22228, AG023185, K08AG022228, U01AG016976, P50AG005131, AG-O5131, R01AG023185)
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-beta isoforms, amyloid-beta 42, Aβ40, amyloid-beta oligomers, amyloid plaques, familial Alzheimer's disease, sporadic Alzheimer's disease, amyloid precursor protein mutations, hippocampus, cerebral cortex, cerebellum
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Humans, Male, Middle Aged, Peptide Fragments, Mass Spectrometry, Statistics as Topic, Amyloid beta-Peptides, Protein Isoforms, Immunoprecipitation

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Mass spectrometric characterization of brain amyloid beta isoform signatures in familial and sporadic Alzheimer’s disease

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