Nitric oxide (NO) is an endogenously synthesized free radical involved in a plethora of physiological phenomena affecting cardiovascular homeostasis and neural functions. Its unregulated bioavailability has been recognized as a key factor in neurodegenerative disorders, especially in relation to the mechanisms through which NO-mediated vascular impairment accentuates the effect of reactive oxygen species. Interestingly, the recent literature indicates the pivotal role of NO and oxidative stress to both early and advanced stages of neurodegenerative disorders, as well as promoting their progression. Alzheimer’s disease (AD) is the most common form of dementia, characterized by extracellular amyloid (Aβ) plaques and intracellular neurofibrillary tangles coupled with reactive microgliosis and the loss of neurons and synapses in the cortex. However, the recent research supports the hypothesis of the pivotal role of NO depletion in the reduction of extracranial blood flow and impairment of cortical and peripheral circulation with a consequent detriment of cognitive function in humans with AD. It is worth of mention that AD, the leading form of dementia, continues to elude the scientific “armada” devoted on fighting this disruptive neurodegenerative disease, particularly with respect to its multifaceted origin. Although research on the biological mechanisms underlying the cause and the progression of AD is advancing, we are far to discover effective therapeutics or disease-modifying approaches. Currently, there is no absolute cure for AD: the few drugs available simply lessen the clinical symptoms. Therefore, new therapeutic approaches, including NO homeostasis, should be considered and might be useful as therapeutic targets.

Chapter 11: The role of nitric oxide on vascular dysfunction during aging and Alzheimer’s disease.

Venturelli, Massimo
2019-01-01

Abstract

Nitric oxide (NO) is an endogenously synthesized free radical involved in a plethora of physiological phenomena affecting cardiovascular homeostasis and neural functions. Its unregulated bioavailability has been recognized as a key factor in neurodegenerative disorders, especially in relation to the mechanisms through which NO-mediated vascular impairment accentuates the effect of reactive oxygen species. Interestingly, the recent literature indicates the pivotal role of NO and oxidative stress to both early and advanced stages of neurodegenerative disorders, as well as promoting their progression. Alzheimer’s disease (AD) is the most common form of dementia, characterized by extracellular amyloid (Aβ) plaques and intracellular neurofibrillary tangles coupled with reactive microgliosis and the loss of neurons and synapses in the cortex. However, the recent research supports the hypothesis of the pivotal role of NO depletion in the reduction of extracranial blood flow and impairment of cortical and peripheral circulation with a consequent detriment of cognitive function in humans with AD. It is worth of mention that AD, the leading form of dementia, continues to elude the scientific “armada” devoted on fighting this disruptive neurodegenerative disease, particularly with respect to its multifaceted origin. Although research on the biological mechanisms underlying the cause and the progression of AD is advancing, we are far to discover effective therapeutics or disease-modifying approaches. Currently, there is no absolute cure for AD: the few drugs available simply lessen the clinical symptoms. Therefore, new therapeutic approaches, including NO homeostasis, should be considered and might be useful as therapeutic targets.
9780128165454
Circulation; Aging; Alzheimer’s disease; Nitric oxide; Vascular dysfunction
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/993969
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact