Biological Bases of Alzheimer's Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (1 July 2024) | Viewed by 1725

Special Issue Editors


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Guest Editor
Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, 171 64 Solna, Sweden
Interests: endocannabinoid system; Alzheimer’s; amyloid; inflammation; microglia; animal models; transmembrane proteins
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Guest Editor
Department of Molecular and Translational Medicine, Division of Pharmacology, University of Brescia, 25123 Brescia, Italy
Interests: secondary metabolites; ethnopharmacology; abiotic stress; abiotic stress tolerance; cannabis sativa; cannabaceae; medical marijuana; phytocannabinoids; CB1 receptor; cannabidiol; tetrahydrocannabinol; CB2 receptor; cannabinoids; cannabinoid receptor agonists; cannabinoid receptor antagonists; cannabinoid receptor modulators
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's Disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia, characterized by impaired memory, cognition, and functionality in affected individuals. Its histological hallmarks consist of brain extracellular deposits of amyloid-beta (Aβ) plaques and intracellular neurofibrillary tangles of tau proteins. Although AD is a multifactorial disease, the main biological basis theory centers on the aberrant processing and accumulation of Aβ peptides, triggering neuronal damage and death. Genetic factors, such as mutations in APP, PSEN1, and PSEN2 genes, have been implicated in early onset familial AD, while polymorphisms in the APOE gene are a risk factor for late-onset AD. In addition to these molecular and genetic underpinnings, other biological factors such as oxidative stress, inflammation, and impaired brain metabolism play pivotal roles in disease progression. Despite the complexity of its etiology, recent advancements in neuroscience and molecular biology have provided promising routes for novel diagnostic markers and therapeutic strategies. Understanding the biological mechanisms of AD is critical to addressing the increasing number of people worldwide affected by this devastating disease.

This Special Issue welcomes submissions of original research articles, reviews, and short communications focusing on the biological mechanisms underlying the onset of AD to increase our understanding of its pathophysiology and contribute to the identification of new biological mechanisms that can be potentially targeted for its treatment.

Dr. Simone Tambaro
Prof. Dr. Andrea Mastinu
Guest Editors

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Keywords

  • Alzheimer's disease
  • amyloid-beta (Aβ) plaques
  • neurofibrillary tangles
  • neuroinflammation
  • biological mechanisms
  • APP
  • PSEN
  • memory impairment
 

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Published Papers (1 paper)

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Research

16 pages, 5467 KiB  
Article
Huperzine A Regulates the Physiological Homeostasis of Amyloid Precursor Protein Proteolysis and Tau Protein Conformation—A Computational and Experimental Investigation
by Suwakon Wongjaikam, Chutikorn Nopparat, Parichart Boontem, Jiraporn Panmanee, Nopporn Thasana, Mayuri Shukla and Piyarat Govitrapong
Biology 2024, 13(7), 518; https://doi.org/10.3390/biology13070518 - 12 Jul 2024
Viewed by 1251
Abstract
The beneficial actions of the natural compound Huperzine A (Hup A) against age-associated learning and memory deficits promote this compound as a nootropic agent. Alzheimer’s disease (AD) pathophysiology is characterized by the accumulation of amyloid beta (Aβ). Toxic Aβ oligomers account for the [...] Read more.
The beneficial actions of the natural compound Huperzine A (Hup A) against age-associated learning and memory deficits promote this compound as a nootropic agent. Alzheimer’s disease (AD) pathophysiology is characterized by the accumulation of amyloid beta (Aβ). Toxic Aβ oligomers account for the cognitive dysfunctions much before the pathological lesions are manifested in the brain. In the present study, we investigated the effects of Hup A on amyloid precursor protein (APP) proteolysis in SH-SY5Y neuroblastoma cells. Hup A downregulated the expression of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) and presenilin 1 (PS1) levels but augmented the levels of A disintegrin and metalloproteinase 10 (ADAM10) with significant decrement in the Aβ levels. We herein report for the first time an in silico molecular docking analysis that revealed that Hup A binds to the functionally active site of BACE1. We further analyzed the effect of Hup A on glycogen synthase kinase-3 β (GSK3β) and phosphorylation status of tau. In this scenario, based on the current observations, we propose that Hup A is a potent regulator of APP processing and capable of modulating tau homeostasis under physiological conditions holding immense potential in preventing and treating AD like disorders. Full article
(This article belongs to the Special Issue Biological Bases of Alzheimer's Disease)
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