Sci Transl Med: LRRK2 mediates small glial cytotoxicity through NFATc2 synactogenesis.

Synactal nuclear disease (Synucleinopathies) is a class of neurodegenerative diseases characterized by abnormal deposition of α-synactal nucleoproteins, including Parkinson's disease, Louisian dementia, and multisyscular atrophy.
these diseases also have neuron loss and neuro-inflammation.
-syn α actoid nucleoproteins released by neurons induce neurotoxic, inflammation-promoting small glial cell reactions through Toll-like subject 2, but their molecular mechanisms are unclear.
study, researchers found that repetitive kinase 2 (LRRK2), rich in leucine, played a key role in activating small glial cells in extracellular α-synth nucleoproteins.
α-synth nucleoproteins released by neurons activate small glial cell LRRK2 Studies have shown that exposure to α-synactins enhances LRRK2 phosphate and activity in primary glial cells in mice.
In addition, genetic and drug-inhibited LRRK2 significantly reduced the toxicity of small glial cytotoxicities mediated by reducing the expression of tumor necrotogens α-α and leurium melebin-6 in mouse cultures.
the nuclear transsexual researchers who regulate NFATc2 in LRRK2 have experimentally verified that LRRK2 promotes neural inflammatory cascading responses by selectively phosphating and inducing the nuclear transsexualization of the immunotransviral factor nuclei factor 2 (NFATc2) of active T cells.
inhibition of LRRK2 can alleviate neuropathy NFATc2 in mouse models of synapse nucleopathy, which is found in synactosurf patients and syngenta mouse models, in which LRRK2 inhibitors are given to restore their motor behavior defects.
, the results suggest that the regulation of LRRK2 and its downstream signaling molecule, NFATc2, may be a target for the treatment of synactopathy.
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