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
Interests: endocannabinoid system; Alzheimer’s; amyloid; inflammation; microglia; animal models; transmembrane proteins
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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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