About this Research Topic
Alzheimer’s disease (AD) is a prevalent age-related neurodegenerative disorder characterized by progressive synaptic and cognitive impairments, making it the leading cause of dementia. A defining pathological hallmark of AD is the abnormal accumulation of cerebral amyloid-β (Aβ), which results from the proteolytic processing of the β-amyloid precursor protein by β- and γ-secretases. The toxicity of Amyloid-β is multifaceted, contributing to synaptic impairment, excitotoxicity, membrane permeability alterations, disrupted calcium homeostasis, inflammation, oxidative stress, and mitochondrial dysfunction. Despite the focus on the amyloid hypothesis in AD drug development, which aims to reduce Aβ production or enhance its clearance, there remains a significant gap in understanding the precise mechanisms of Aβ toxicity and its impact on brain functions and behavior. Recent studies have advanced our knowledge, yet a comprehensive understanding of these processes is crucial for developing effective therapeutic strategies.
This Research Topic aims to delve into the toxicity of Amyloid-β on brain functions and their subsequent effects on behavior. By compiling a collection of original research articles, reviews, and opinion pieces, this initiative seeks to uncover the mechanisms underlying Aβ toxicity and its influence on cognition and behavior. The ultimate goal is to pave the way for innovative therapeutic strategies that optimize the prevention and treatment of Alzheimer's disease.
To gather further insights into the effects of Amyloid-β on brain functions and behavior, we welcome articles addressing, but not limited to, the following themes:
- In vivo studies on AD animal models, such as rodents and non-human primates, to illustrate Aβ toxicity and memory deficits.
- In vitro studies to elucidate the effects of Aβ and the underlying cellular and molecular mechanisms.
- Development and use of innovative techniques, including nanoparticle carriers, shRNA knockdown, and anti-Aβ antibodies, to demonstrate the potential benefits of reducing Aβ on synaptic plasticity and memory deficits in AD animal models.
This Research Topic aims to delve into the toxicity of Amyloid-β on brain functions and their subsequent effects on behavior. By compiling a collection of original research articles, reviews, and opinion pieces, this initiative seeks to uncover the mechanisms underlying Aβ toxicity and its influence on cognition and behavior. The ultimate goal is to pave the way for innovative therapeutic strategies that optimize the prevention and treatment of Alzheimer's disease.
To gather further insights into the effects of Amyloid-β on brain functions and behavior, we welcome articles addressing, but not limited to, the following themes:
- In vivo studies on AD animal models, such as rodents and non-human primates, to illustrate Aβ toxicity and memory deficits.
- In vitro studies to elucidate the effects of Aβ and the underlying cellular and molecular mechanisms.
- Development and use of innovative techniques, including nanoparticle carriers, shRNA knockdown, and anti-Aβ antibodies, to demonstrate the potential benefits of reducing Aβ on synaptic plasticity and memory deficits in AD animal models.
Keywords: Abeta peptide, brain function, behavior, oligomers, toxicity, memory deficits, trafficking, prion knockdown, nanoparticles, shRNA, oligomer aggregates
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
