New insights into sodium phenylbutyrate as a pharmacotherapeutic option for neurological disorders.
Daniel JuarezAnabella Handal-SilvaJose Luis Morán-PeralesDiana M Torres-CifuentesGonzalo FloresSamuel TreviñoAlbino Moreno-RodriguezJorge GuevaraAlfonso Diaz-FonsecaePublished in: Synapse (New York, N.Y.) (2024)
Neurological disorders (NDs) are diseases of the central and peripheral nervous systems that affect more than one billion people worldwide. The risk of developing an ND increases with age due to the vulnerability of the different organs and systems to genetic, environmental, and social changes that consequently cause motor and cognitive deficits that disable the person from their daily activities and individual and social productivity. Intrinsic factors (genetic factors, age, gender) and extrinsic factors (addictions, infections, or lifestyle) favor the persistence of systemic inflammatory processes that contribute to the evolution of NDs. Neuroinflammation is recognized as a common etiopathogenic factor of ND. The study of new pharmacological options for the treatment of ND should focus on improving the characteristic symptoms and attacking specific molecular targets that allow the delay of damage processes such as neuroinflammation, oxidative stress, cellular metabolic dysfunction, and deregulation of transcriptional processes. In this review, we describe the possible role of sodium phenylbutyrate (NaPB) in the pathogenesis of Alzheimer's disease, hepatic encephalopathy, aging, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis; in addition, we describe the mechanism of action of NaPB and its beneficial effects that have been shown in various in vivo and in vitro studies to delay the evolution of any ND.
Keyphrases
- oxidative stress
- amyotrophic lateral sclerosis
- mental health
- healthcare
- climate change
- traumatic brain injury
- physical activity
- cerebral ischemia
- metabolic syndrome
- gene expression
- cardiovascular disease
- cognitive impairment
- dna damage
- ischemia reperfusion injury
- weight loss
- single molecule
- early onset
- blood brain barrier
- transcription factor
- subarachnoid hemorrhage
- induced apoptosis
- combination therapy
- smoking cessation
- sleep quality