New insights on the potential effect of vinpocetine in Parkinson’s disease: one of the neglected warden and baffling topics

Abstract

Vinpocetine (VPN) is an ethyl apovincaminate that has anti-inflammatory and antioxidant effects by inhibiting the expression of nuclear factor kappa B (NF-κB) and phosphodiesterase enzyme 1 (PDE-1). VPN is used in the management of stroke, dementia, and other neurodegenerative brain diseases. VPN may be effective in treating Parkinson’s disease (PD). Therefore, this review aimed to clarify the mechanistic role of VPN in the management of PD. VPN has protective and restorative effects against neuronal injury by reducing neuroinflammation, and improvement of synaptic plasticity and cerebral blood flow. VPN protects dopaminergic neurons by reducing oxidative stress, lipid peroxidation, glutamate neurotoxicity, and regulation of Ca+ 2 overloads. VPN can alleviate PD neuropathology through its anti-inflammatory, antioxidant, antiapoptotic and neurogenic effects. VPN through inhibition of PDE1 improves cyclic adenosine monophosphate (cAMP)/cyclic guanosine monophosphate (cGMP) signaling in the dopaminergic neurons of the substantia nigra (SN). VPN improves PD neuropathology through PDE1 inhibition with a subsequent increase of the cAMP/cGMP signaling pathway. Therefore, increasing cAMP leads to antioxidant effects, while augmentation of cGMP by VPN leads to anti-inflammatory effects which reduced neurotoxicity and development of motor severity in PD. In conclusion, this review indicated that VPN could be effective in the management of PD.

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“…The mechanism of α‐synuclein‐induced neurodegeneration is not well understood. However, the formation of neurotoxic α‐synuclein filaments might be the possible mechanism 126 . It has been shown that epilepsy and neurodegenerative diseases such as AD and PD share a frequent underlying mechanism 127 .…”

“…However, the formation of neurotoxic α‐synuclein filaments might be the possible mechanism. 126 It has been shown that epilepsy and neurodegenerative diseases such as AD and PD share a frequent underlying mechanism. 127 Released α‐synuclein from injured neurons activates astrocytes and microglia leading to neuroinflammation and degeneration of inhibitory neurotransmitters with subsequent induction of epileptogenesis.…”

The potential role of brain renin‐angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?

“…Besides, the activated microglia triggers the activation of astrocytes which also promote the expression and the release of pro‐inflammatory cytokines. 13 , 14 Mutated Parkin, PINK1 and DJ‐1 genes that induce mitochondrial dysfunction together with mutant α‐Syn and the extracellular neuromelanin from damaged dopaminergic neurons contribute in the activation of microglia and the development of neurodegeneration in the SN, 12 , 13 , 15 , 16 , 17 (Figure 1 ).…”