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Plasma IAPP-autoantibody levels in Alzheimer’s disease patients are affected by APOE4 status
Cognitive Disorder Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Department of Internal Medicine, Lund University, Skåne University Hospital, Malmö, Sweden.
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Cognitive Disorder Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
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2023 (Engelska)Ingår i: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 24, nr 4, artikel-id 3776Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Pancreas-derived islet amyloid polypeptide (IAPP) crosses the blood–brain barrier and co-deposits with amyloid beta (Aβ) in brains of type 2 diabetes (T2D) and Alzheimer’s disease (AD) patients. Depositions might be related to the circulating IAPP levels, but it warrants further investigation. Autoantibodies recognizing toxic IAPP oligomers (IAPPO) but not monomers (IAPPM) or fibrils have been found in T2D, but studies on AD are lacking. In this study, we have analyzed plasma from two cohorts and found that levels of neither immunoglobulin (Ig) M, nor IgG or IgA against IAPPM or IAPPO were altered in AD patients compared with controls. However, our results show significantly lower IAPPO-IgA levels in apolipoprotein E (APOE) 4 carriers compared with non-carriers in an allele dose-dependent manner, and the decrease is linked to the AD pathology. Furthermore, plasma IAPP-Ig levels, especially IAPP-IgA, correlated with cognitive decline, C-reactive protein, cerebrospinal fluid Aβ and tau, neurofibrillary tangles, and brain IAPP exclusively in APOE4 non-carriers. We speculate that the reduction in IAPPO-IgA levels may be caused by increased plasma IAPPO levels or masked epitopes in APOE4 carriers and propose that IgA and APOE4 status play a specific role in clearance of circulatory IAPPO, which may influence the amount of IAPP deposition in the AD brain.

Ort, förlag, år, upplaga, sidor
MDPI, 2023. Vol. 24, nr 4, artikel-id 3776
Nyckelord [en]
AD, amylin, amyloid beta, APOE4, autoantibodies, cognition, IgA, IgG, IgM, T2D
Nationell ämneskategori
Neurologi
Identifikatorer
URN: urn:nbn:se:umu:diva-205645DOI: 10.3390/ijms24043776ISI: 000944882900001Scopus ID: 2-s2.0-85149143255OAI: oai:DiVA.org:umu-205645DiVA, id: diva2:1743050
Forskningsfinansiär
Vetenskapsrådet, 2018-02564Hjärnfonden, FO2022-0039Olle Engkvists stiftelse, 194-643Lunds universitetVetenskapsrådet, 2022-00775Knut och Alice Wallenbergs Stiftelse, 2017-0383Alzheimerfonden, AF-980907Hjärnfonden, FO2021-0293Parkinsonfonden, 1412/22Konung Gustaf V:s och Drottning Victorias FrimurarestiftelseKempestiftelsernaTillgänglig från: 2023-03-13 Skapad: 2023-03-13 Senast uppdaterad: 2023-09-05Bibliografiskt granskad

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Olofsson, Anders

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