Impaired dopamine release in Parkinson’s disease

Abstract

Parkinson’s disease is the second most common neurodegenerative disease and yet the early pathophysiological events of the condition and sequences of dysfunction remain unclear. The loss of dopaminergic neurons and reduced levels of striatal dopamine are descriptions used interchangeably as underlying the motor deficits in Parkinson’s Disease. However, decades of research suggest that dopamine release deficits in Parkinson’s Disease do not occur only after cell death, but that there is dysfunction or dysregulation of axonal dopamine release before cell loss. Here we review the evidence for dopamine release deficits prior to neurodegeneration in Parkinson’s Disease, drawn from a large and emerging range of Parkinson’s Disease models, and the mechanisms by which these release deficits occur. The evidence indicates that impaired dopamine release can result from disruption to a diverse range of Parkinson’s Disease-associated genetic and molecular disturbances, and can be considered as a potential pathophysiological hallmark of Parkinson’s Disease.

Gastrodia elata polysaccharide alleviates Parkinson's disease via inhibiting apoptotic and inflammatory signaling pathways and modulating the gut microbiota

“…The accumulation and deposition of Lewy bodies are closely related to the increase in the death level of DA neurons. 69 α-SYN is the main protein in Lewy bodies. The accumulation of α-SYN in PD patients is higher than that in healthy individuals, and this phenomenon is also observed in MPTP-induced animal models such as monkey, mouse, and silkworm.…”

Co Single-Atom Nanozymes for the Simultaneous Electrochemical Detection of Uric Acid and Dopamine in Biofluids

“…6,7 As the most abundant catecholamine neurotransmitter in the brain, dopamine regulates the central nervous system. The abnormal concentration of dopamine can cause neurological disorders such as Parkinson's disease, 8,9 schizophrenia, 10 and Tourette's syndrome. 11 Fascinatingly, it has been shown that uric acid has a protective effect on dopamine neurons in Parkinson's disease and that uric acid levels affect the course of Parkinson's disease.…”

“…A delicate dynamic balance is maintained through production and excretion. , Once the balance is disturbed, it can lead to a variety of diseases, such as hyperuricemia, gout, , and cardiovascular system diseases. , As the most abundant catecholamine neurotransmitter in the brain, dopamine regulates the central nervous system. The abnormal concentration of dopamine can cause neurological disorders such as Parkinson’s disease, , schizophrenia, and Tourette’s syndrome …”

Striatal dopamine depletion drives disease progression and network topology aberrations specifically by impairing left M1 network

“…1,2 One of the most prominent pathological hallmarks of PD is the loss of dopaminergic neurons in the substantia nigra, 3 resulting in the deficiency of dopamine in the striatum. 4 Dopamine transporter imaging using single-photon emission computed tomography (DAT-SPECT) is one of the most highly developed supplementary assessments for PD, which is utilized to indirectly measure DAT availability in straitum. 5,6 Striatal binding ratio (SBR) in striatum measured by DAT-SPECT has been demonstrated to be associated with motor manifestations, including rigidity, 7,8 resting tremor, 9 and bradykinesia.…”