Unravelling Interactions between Amyloid Beta (Aβ) and Key Pathological Features of Alzheimer’s Disease

Dear Colleagues,

The recent successful trials of amyloid beta (Aβ) immunotherapies in early Alzheimer’s disease (AD) patients demonstrate that the removal of brain amyloid leads to modest, yet evident, clinical benefits. In addition, anti-amyloid treatments appear to modify the complicated underlying pathophysiology of AD, improving biomarkers related to soluble and insoluble tau pathology and neuroinflammation. These clinical data highlight the pivotal role of Aβ in AD pathogenesis and raise important questions regarding its interplay with other main features of the disorder. How do Aβ accumulation and clearance impact the downstream molecular pathways associated with hallmark AD pathology, and to what extent? Are there potential synergistic effects of combining therapies against multiple AD-related processes? How do the complex interactions of Aβ with other AD lesions differ across different disease stages? This Special Issue will explore the molecular interactions between Aβ and the rest of the defining features of AD, such as tau pathology, neuroinflammation, synaptic dysfunction, energy metabolism, and related mechanisms. By fostering a deeper understanding of the interplay between multiple AD processes, we hope to uncover potential therapeutic targets and innovative strategies for tackling this devastating disease.

This special issue is supervised by Dr. Athanasios Metaxas and assisted by our Topical Advisory Panel Member Dr. Malamati Kourti （European University Cyprus, Nicosia, Cyprus).

Dr. Athanasios Metaxas
Guest Editor

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• Alzheimer’s disease
• amyloid
• tau
• neuroinflammation
• synapses
• metabolism