About this Research Topic
Neurodegenerative diseases are among the main chronic illnesses and the first cause of mortality and disability worldwide. They include a spectrum of clinical disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), Cerebrovascular disease (CeVD), Huntington disease (HD), and Vascular Dementia (VD), among others.
Despite a great scientific effort to improve pharmacological treatment and prevention, an effective therapy against neurodegenerative diseases has not been discovered so far.
The principal mechanism leading to all neurodegenerative diseases is neurodegeneration, defined as a progressive and inexorable death of neurons and loss in neuronal function. Neurodegeneration may be induced by complex and multifactorial processes, which usually are a combination of vascular, environmental and genetic factors.
Hopefully, a better understanding of the biology of neurodegeneration and the interactions between the factors leading to it, may allow to develop novel and more efficient pharmacotherapies.
Strong evidence suggests that changes in the heart, peripheral and cerebral blood flow hemodynamic have a functional role in the development of neurodegenerative and cognitive diseases.
Alterations in cerebral blood flow (CBF) due to change in large cerebral blood vessels, such as carotid arteries, have been associated with an increase in the risk for cognitive decline and AD. Different phenotypes of carotid atherosclerosis, like carotid intima media thickness (IMT) and carotid stiffness, have been linked with major markers of neurodegeneration, such as white matter hyperintensities (WMH) and amyloid-β peptide accumulation.
Heart failure, by controlling the CBF directly, has been demonstrated to be correlated with risk for cognitive decline. Impairment in heart function (e.g. chronic arrhythmia) along with increase in vascular peripheral resistance further promote the disruption of cerebral microvessels and formation of microemboli.
Several have been the proposed mediators underlying the association between impairment in vascular homeostasis and neurodegeneration, including endothelial factors, nitric oxide (NO), mitochondrial respiration, oxidative stress and inflammation.
Based on these previous evidences, therapies for vascular disease cure and prevention, as statins, antihypertensive, and antidiabetic drugs, have been already proposed and tested as candidates to treat neurodegenerative diseases - especially drugs related to specific molecular pathways discusses above. However, so far, the neurodegenerative diseases are incurable. The investigation of pathological processes linking CBF with progression of neurodegeneration and cognitive decline may be an opportunity for drug repurposing (also known as drug repositioning or drug reprofiling) and to discovery novel therapies targeting both vascular and neurodegenerative diseases.
This Research Topic will focus on providing an overview in the current knowledge on the mechanisms underlying the link between central and peripheral blood flow hemodynamic and neurodegeneration, with the special emphasis on the current and most promising therapies in this field.
Possible studies discussing vascular and environmental risk factors, genetic variants, and molecular pathways implicated in this association, along with discussion on drugs or compounds affecting them, are welcome. We also welcome Original Research papers, Review articles and brief communications addressing the same field.
Despite a great scientific effort to improve pharmacological treatment and prevention, an effective therapy against neurodegenerative diseases has not been discovered so far.
The principal mechanism leading to all neurodegenerative diseases is neurodegeneration, defined as a progressive and inexorable death of neurons and loss in neuronal function. Neurodegeneration may be induced by complex and multifactorial processes, which usually are a combination of vascular, environmental and genetic factors.
Hopefully, a better understanding of the biology of neurodegeneration and the interactions between the factors leading to it, may allow to develop novel and more efficient pharmacotherapies.
Strong evidence suggests that changes in the heart, peripheral and cerebral blood flow hemodynamic have a functional role in the development of neurodegenerative and cognitive diseases.
Alterations in cerebral blood flow (CBF) due to change in large cerebral blood vessels, such as carotid arteries, have been associated with an increase in the risk for cognitive decline and AD. Different phenotypes of carotid atherosclerosis, like carotid intima media thickness (IMT) and carotid stiffness, have been linked with major markers of neurodegeneration, such as white matter hyperintensities (WMH) and amyloid-β peptide accumulation.
Heart failure, by controlling the CBF directly, has been demonstrated to be correlated with risk for cognitive decline. Impairment in heart function (e.g. chronic arrhythmia) along with increase in vascular peripheral resistance further promote the disruption of cerebral microvessels and formation of microemboli.
Several have been the proposed mediators underlying the association between impairment in vascular homeostasis and neurodegeneration, including endothelial factors, nitric oxide (NO), mitochondrial respiration, oxidative stress and inflammation.
Based on these previous evidences, therapies for vascular disease cure and prevention, as statins, antihypertensive, and antidiabetic drugs, have been already proposed and tested as candidates to treat neurodegenerative diseases - especially drugs related to specific molecular pathways discusses above. However, so far, the neurodegenerative diseases are incurable. The investigation of pathological processes linking CBF with progression of neurodegeneration and cognitive decline may be an opportunity for drug repurposing (also known as drug repositioning or drug reprofiling) and to discovery novel therapies targeting both vascular and neurodegenerative diseases.
This Research Topic will focus on providing an overview in the current knowledge on the mechanisms underlying the link between central and peripheral blood flow hemodynamic and neurodegeneration, with the special emphasis on the current and most promising therapies in this field.
Possible studies discussing vascular and environmental risk factors, genetic variants, and molecular pathways implicated in this association, along with discussion on drugs or compounds affecting them, are welcome. We also welcome Original Research papers, Review articles and brief communications addressing the same field.
Keywords: Blood Flow, Heart Failure, Cerebrovascular Homeostasis, Neurodegeneration, Atherosclerosis
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