Background
Type: Review

The neuroprotective effects of ferulic acid in toxin-induced models of Parkinson's disease: A review

Journal: Ageing Research Reviews (15681637)Year: 2024/06/01Volume: 97Issue:
Hassani S.Esmaeili A.a
DOI:10.1016/j.arr.2024.102299Language: English

Abstract

Parkinson's disease is predominantly caused by dopaminergic neuron loss in the substantia nigra pars compacta and the accumulation of alpha-synuclein protein. Though the general consensus is that several factors, such as aging, environmental factors, mitochondrial dysfunction, accumulations of neurotoxic alpha-synuclein, malfunctions of the lysosomal and proteasomal protein degradation systems, oxidative stress, and neuroinflammation, are involved in the neurodegeneration process of Parkinson's disease, the precise mechanism by which all of these factors are triggered remains unknown. Typically, neurotoxic compounds such as rotenone, 6-hydroxydopamine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl 4-phenyl pyridinium (mpp+), paraquat, and maneb are used to Preclinical models of Parkinson's disease Ferulic acid is often referred to by its scientific name, 4-hydroxy-3-methoxycinnamic acid (C10H10O4), and is found naturally in cereals, fruits, vegetables, and bee products. This substance exhibits neuroprotective effects against Parkinson's disease because of its intriguing potential, which includes anti-inflammatory and antioxidant qualities. This review goes into additional detail about Parkinson's disease and the neuroprotective properties of ferulic acid that may help prevent the condition. © 2024 Elsevier B.V.


Author Keywords

Ferulic acidMitochondrial disordersNeuroinflammationOxidative stressParkinson's disease

Other Keywords

AnimalsCoumaric AcidsDisease Models, AnimalHumansNeuroprotective AgentsParkinson Diseasealpha synucleinferulic acidironnanoparticleneurotoxinneurotransmittertoxincoumaric acidneuroprotective agentantiapoptotic activityantiinflammatory activityantioxidant activityblood brain barriercell deathcell viabilityDNA fragmentationdopaminergic nerve cellhumaninflammationmitochondrial biogenesismitochondrial dynamicsmitochondrial membrane potentialmitochondrionneuroprotectionneurotoxicitynonhumanoxidative stresspHpharmacokinetic parameterspromoter regionReviewanimaldisease modelmetabolismpathology