β-Amyloids and Immune Responses Associated with Alzheimer's Disease

• Published in: Cells (Basel, Switzerland) Switzerland), 2024-09, Vol.13 (19), p.1624
• Main Authors: Kolobova, Elizaveta, Petrushanko, Irina, Mitkevich, Vladimir, Makarov, Alexander A, Grigorova, Irina L
• Format: Article
• Language: English
• Subjects: Adaptive Immunity; Advertising executives; Aggregates; Alzheimer Disease - immunology; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid beta-Peptides - immunology; Amyloid beta-Peptides - metabolism; Animals; antibody; Antigens; B cells; B-Lymphocytes - immunology; B-Lymphocytes - metabolism; Brain; Cognitive ability; Cytotoxicity; Development and progression; Diseases; Glycoproteins; Humans; Hypotheses; Immune response; Immunity, Innate; Isoforms; Lymphocytes; Lymphocytes B; Membranes; Mutation; Neurodegeneration; Neurodegenerative diseases; Neurotoxicity; Oligomerization; Oligomers; Pathogenesis; Pathology; Peptides; post-translational modifications of β-amyloid; Review; Senile plaques; T cell receptors; Toxicity; β-Amyloid
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells13191624

Alzheimer's disease (AD) is associated with the accumulation of β-amyloids (Aβs) and the formation of Aβ plaques in the brain. Various structural forms and isoforms of Aβs that have variable propensities for oligomerization and toxicity and may differentially affect the development of AD have been identified. In addition, there is evidence that β-amyloids are engaged in complex interactions with the innate and adaptive immune systems, both of which may also play a role in the regulation of AD onset and progression. In this review, we discuss what is currently known about the intricate interplay between β-amyloids and the immune response to Aβs with a more in-depth focus on the possible roles of B cells in the pathogenesis of AD.