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

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1858

Special Issue Editor


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Guest Editor
Department of Life Sciences, School of Sciences, European University Cyprus, 6 Diogenis Str., Nicosia 1516, Cyprus
Interests: disease modeling; behavioral and cognitive neuroscience; pharmacology, imaging, Alzheimer’s disease

Special Issue Information

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

Manuscript Submission Information

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Keywords

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

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Published Papers (1 paper)

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Review

31 pages, 1836 KiB  
Review
A Comprehensive Exploration of the Multifaceted Neuroprotective Role of Cannabinoids in Alzheimer’s Disease across a Decade of Research
by Petros Tyrakis, Christina Agridi and Malamati Kourti
Int. J. Mol. Sci. 2024, 25(16), 8630; https://doi.org/10.3390/ijms25168630 - 7 Aug 2024
Viewed by 1373
Abstract
Alzheimer’s disease (AD), a progressive neurodegenerative disorder, manifests through dysregulation of brain function and subsequent loss of bodily control, attributed to β-amyloid plaque deposition and TAU protein hyperphosphorylation and aggregation, leading to neuronal death. Concurrently, similar cannabinoids to the ones derived from Cannabis [...] Read more.
Alzheimer’s disease (AD), a progressive neurodegenerative disorder, manifests through dysregulation of brain function and subsequent loss of bodily control, attributed to β-amyloid plaque deposition and TAU protein hyperphosphorylation and aggregation, leading to neuronal death. Concurrently, similar cannabinoids to the ones derived from Cannabis sativa are present in the endocannabinoid system, acting through receptors CB1R and CB2R and other related receptors such as Trpv-1 and GPR-55, and are being extensively investigated for AD therapy. Given the limited efficacy and adverse effects of current available treatments, alternative approaches are crucial. Therefore, this review aims to identify effective natural and synthetic cannabinoids and elucidate their beneficial actions for AD treatment. PubMed and Scopus databases were queried (2014–2024) using keywords such as “Alzheimer’s disease” and “cannabinoids”. The majority of natural (Δ9-THC, CBD, AEA, etc.) and synthetic (JWH-133, WIN55,212-2, CP55-940, etc.) cannabinoids included showed promise in improving memory, cognition, and behavioral symptoms, potentially via pathways involving antioxidant effects of selective CB1R agonists (such as the BDNF/TrkB/Akt pathway) and immunomodulatory effects of selective CB2R agonists (TLR4/NF-κB p65 pathway). Combining anticholinesterase properties with a cannabinoid moiety may enhance therapeutic responses, addressing cholinergic deficits of AD brains. Thus, the positive outcomes of the vast majority of studies discussed support further advancing cannabinoids in clinical trials for AD treatment. Full article
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