Alzheimer’s disease (AD), the most common cause of dementia, is an age-dependent neurodegenerative disorder with progressive impairments in synaptic and cognitive functions. A disease-defining pathological hallmark of AD is the abnormal accumulation of cerebral amyloid-β (Aβ), which is formed by the sequential proteolytic processing of the β-amyloid precursor protein by β- and γ-secretases.
The toxicity of Aβ oligomers includes but is not limited to, synaptic impairment, excitotoxicity, alterations in membrane permeability, altered calcium homeostasis, inflammation, oxidative stress, and mitochondrial abnormalities. AD drug development is driven mainly by the amyloid hypothesis, and therapies that reduce Aβ production or increase Aβ clearance are therefore potential disease-modifying strategies.
This Research Topic aims to explore the toxicity of Aβ oligomers on brain functions and their subsequent impact on brain behavior. The resulting collection of cutting-edge original research articles, reviews, and opinion pieces will provide valuable insights into the mechanisms underlying Aβ toxicity and its impact on cognition and behavior.
Research outputs and advanced methodological approaches will pave the way for innovative therapeutic strategies aimed at optimizing Alzheimer's disease prevention and treatment.
To build up a consolidated collection of articles tackling the impact of Aβ oligomers on brain functions and behavior, and to develop targeted future treatment strategies, we welcome:
· In vivo studies performed on AD animal models (rodents, non-human primates, etc.) to illustrate Aβ toxicity and memory deficits.
· In vitro studies to elucidate Aβ effect and underlying cellular and molecular mechanisms.
· Development and use of innovative techniques, such as nanoparticle carriers, shRNA knockdown, anti- Aβ antibodies, etc., to illustrate 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.
Alzheimer’s disease (AD), the most common cause of dementia, is an age-dependent neurodegenerative disorder with progressive impairments in synaptic and cognitive functions. A disease-defining pathological hallmark of AD is the abnormal accumulation of cerebral amyloid-β (Aβ), which is formed by the sequential proteolytic processing of the β-amyloid precursor protein by β- and γ-secretases.
The toxicity of Aβ oligomers includes but is not limited to, synaptic impairment, excitotoxicity, alterations in membrane permeability, altered calcium homeostasis, inflammation, oxidative stress, and mitochondrial abnormalities. AD drug development is driven mainly by the amyloid hypothesis, and therapies that reduce Aβ production or increase Aβ clearance are therefore potential disease-modifying strategies.
This Research Topic aims to explore the toxicity of Aβ oligomers on brain functions and their subsequent impact on brain behavior. The resulting collection of cutting-edge original research articles, reviews, and opinion pieces will provide valuable insights into the mechanisms underlying Aβ toxicity and its impact on cognition and behavior.
Research outputs and advanced methodological approaches will pave the way for innovative therapeutic strategies aimed at optimizing Alzheimer's disease prevention and treatment.
To build up a consolidated collection of articles tackling the impact of Aβ oligomers on brain functions and behavior, and to develop targeted future treatment strategies, we welcome:
· In vivo studies performed on AD animal models (rodents, non-human primates, etc.) to illustrate Aβ toxicity and memory deficits.
· In vitro studies to elucidate Aβ effect and underlying cellular and molecular mechanisms.
· Development and use of innovative techniques, such as nanoparticle carriers, shRNA knockdown, anti- Aβ antibodies, etc., to illustrate 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.