Table 1.
Study characteristics. It showcases the main references and findings that demonstrate the connection between LID-NMDAR-neuroinflammation.
| Author | Year | Country | Type of Study | Designof Study | Results |
|---|---|---|---|---|---|
| Angelopoulou et al. | 2021 | Greece | _ | Review | Fyn kinase may regulate LID, enhanced neuroinflammation and glutamate excitotoxicity by mediating NMDAR axes. |
| Azar et al. | 2022 | Egypt | Rat | RCT | Agmatine-mediated inhibition of NMDAR expression and amelioration of dyskinesia with a focus on its anti-inflammatory potentiality. |
| Bartlett et al. | 2020 | USA | Rat | RCT | Ketamine is an NMDAR antagonist.The long-term effects of ketamine depend on BDNF signaling in the striatum. And it attenuates the development of LID in rodents. |
| Bortolanza et al. | 2015 | Brazil | Rat | RCT | Glu are bound to influence microglial activation states. And LID leads to upregulation of iNOS, GFAP and OX-42-ir. |
| Carta et al. | 2017 | Italy | _ | Review | LID and neuroinflammation: microglia and astrocytes play a key role. |
| Cerovic et al. | 2015 | Italy | Mice | RCT | The Ras-ERK signaling has a central role in striatal LTP, depotentiation, and LTP restored after L-DOPA treatment. |
| Chen et al. | 2022 | China | Rat | RCT | Neuroinflammation caused sustained downregulation of synaptic NR2A and NR2B subunits. And anti-inflammatory treatment reversed the downregulation and hypofunction of synaptic NR2A and NR2B. |
| Gurrera | 2019 | USA | Human | RCT | Patients with anti-NMDA receptor encephalitis can develop motor dysfunction. |
| Innes et al. | 2019 | UK | _ | Review | Changes to synaptic plasticity may be mediated by microglial modifications. Microglial production of cytokines may regulate LTP and LTD, thereby underlying the development of disease. |
| Koh et al. | 2022 | South Korea | Mice | RCT | Astrocytes regulate NMDAR tone via BEST1-mediated corelease of D-serine and Glu. |
| Morissette et al. | 2022 | Canada | Monkeys | RCT | Increased inflammatory markers in the basal ganglia associated with LID and revealed that MPEP inhibition of glutamate activity reduced LID and levels of inflammatory markers. |
| Pereira et al. | 2021 | Brazil | Mice | RCT | The release of TNF-α by glutamate-activated astrocytes may contribute to LID by exacerbating corticostriatal glutamatergic inputs excitability and maintaining astrocytes in an activated state through a self-reinforcing mechanism. |
| Rahman et al. | 2022 | Australia | Human | RCT | Neuroinflammation may alter NMDAR stoichiometry, and future studies could aim to determine if anti-inflammatory treatment can alleviate this aspect of NMDAR-related pathology. |
| Rentsch et al. | 2020 | Australia | Mice | RCT | Amantadine, an NMDAR antagonist, may explore novel features of microglia and astrocyte physiology and pathophysiology and their direct and/or indirect impact on neuronal synaptic signalling in LID. |
| Thiele et al. | 2014 | Canada | Mice | RCT | In the LID state, the direct pathway exhibits only LTP, becoming generally overactive, and the indirect pathway exhibits only LTD. |
| Trudler et al. | 2021 | California | Mice | RCT | Glutamate release from astrocytes and excessive extrasynaptic NMDAR activity in neurons, thus contributing to Synapse and neuron Loss. |
| Varley et al. | 2019 | UK | Human | RCT | The Movement disorder associated with NMDAR antibody-encephalitis is complex and characteristic. |
| Wang et al. | 2018 | China | Rat | RCT | CaMKIIa-GluN2B interaction had an important role in the development of LID. CaMKII is also associated with inflammatory pathways. |
| Yan et al. | 2021 | China | Rat | RCT | Systemic inflammation increases the susceptibility to LID in 6-OHDA lesioned rats by targeting the NR2B-Medicated PKC/MEK/ERK Pathway. |
| Yuan et al. | 2023 | China | Rat | RCT | Interventions targeting astrocytes and glutamate transporters may delay LID. |
( Randomized Controlled Trial: RCT. ).