About this Research Topic
The combination of age-related vascular changes, chronic health conditions, inflammation, reduced mobility, and medication use is linked to both microvascular and macrovascular complications in aging individuals and those with dementia. These complications are associated with the accumulation of advanced glycation end products (AGEs), which induce oxidative stress, microglial activation, neuroinflammation, blood-brain barrier (BBB) dysfunction, and abnormal Aβ metabolism. The receptor for AGE (RAGE) is upregulated in brain cells during aging and Alzheimer's disease (AD), correlating with microvascular complications. Age-related neurodegenerative disorders, such as AD, often involve microvascular dysfunction, BBB impairment, neuroinflammation, and neurovascular disintegration. These dysfunctions reduce cerebral blood flow (CBF), impair the clearance of neurotoxic molecules like Aβ, and contribute to the accumulation and aggregation of these molecules, leading to AD pathologies such as cerebral β-amyloidosis and cerebral amyloid angiopathy (CAA).
Vascular aging involves changes in the vascular wall, leading to loss of arterial elasticity and reduced arterial compliance, potentially causing vascular dementia. Vascular dementia, resulting from reduced blood flow to the brain, is the second most common form of dementia after AD, accounting for 20% of cases. It includes conditions like multi-infarct dementia, arising from strokes and other vascular brain injuries that impact memory, thinking, and behavior. RAGE is implicated in the processes of macrovascular and microvascular complications with neurodegeneration, triggering oxidative stress, neurovascular inflammation, and apoptosis, which may lead to vascular aging and dementia. Understanding the mechanisms of AGEs is crucial for developing strategies against vascular aging and related complications.
Increased cerebral vascular permeability allows AGE to cross the BBB and accumulate in the brain, leading to significant upregulation of RAGE and promoting an inflammatory response by vascular endothelial and nerve cells. This response, along with oxidative stress and upregulated AGE-RAGE signaling, contributes to Aβ deposition and generation of reactive oxygen species (ROS), which link to the formation of lipid droplets (LD), inducing inflammation and neuronal apoptosis. The AGE-RAGE axis is thus critical in the pathological changes of AD. However, the effects of AGE accumulation and neurovascular functions in aging or AD are not fully understood.
This special issue aims to:
- Summarize the fundamental role and novel insights into the molecular mechanisms of AGEs in vascular aging and vascular dementia.
- Provide critical evidence on AGEs and vascular dementia differences and the main risk factors of vascular aging.
- Explore pharmaceutical treatments and potential mitigation strategies for risk factors related to vascular aging and vascular dementia.
Vascular aging involves changes in the vascular wall, leading to loss of arterial elasticity and reduced arterial compliance, potentially causing vascular dementia. Vascular dementia, resulting from reduced blood flow to the brain, is the second most common form of dementia after AD, accounting for 20% of cases. It includes conditions like multi-infarct dementia, arising from strokes and other vascular brain injuries that impact memory, thinking, and behavior. RAGE is implicated in the processes of macrovascular and microvascular complications with neurodegeneration, triggering oxidative stress, neurovascular inflammation, and apoptosis, which may lead to vascular aging and dementia. Understanding the mechanisms of AGEs is crucial for developing strategies against vascular aging and related complications.
Increased cerebral vascular permeability allows AGE to cross the BBB and accumulate in the brain, leading to significant upregulation of RAGE and promoting an inflammatory response by vascular endothelial and nerve cells. This response, along with oxidative stress and upregulated AGE-RAGE signaling, contributes to Aβ deposition and generation of reactive oxygen species (ROS), which link to the formation of lipid droplets (LD), inducing inflammation and neuronal apoptosis. The AGE-RAGE axis is thus critical in the pathological changes of AD. However, the effects of AGE accumulation and neurovascular functions in aging or AD are not fully understood.
This special issue aims to:
- Summarize the fundamental role and novel insights into the molecular mechanisms of AGEs in vascular aging and vascular dementia.
- Provide critical evidence on AGEs and vascular dementia differences and the main risk factors of vascular aging.
- Explore pharmaceutical treatments and potential mitigation strategies for risk factors related to vascular aging and vascular dementia.
Keywords: Advanced Glycation End Products (AGEs) Neuroinflammation Blood-brain barrier (BBB) Dysfunction Alzheimer's Disease (AD) Vascular Aging (VA) Vascular Dementia (VD) Receptor for Advanced Glycation End Products (RAGE) Oxidative Stress
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