Traumatic brain injury-induced inflammatory changes in the olfactory bulb disrupt neuronal networks leading to olfactory dysfunction

A Pilot Study on a Possible Mechanism behind Olfactory Dysfunction in Parkinson’s Disease: The Association of TAAR1 Downregulation with Neuronal Loss and Inflammation along Olfactory Pathway

“…In individuals with PD, a specific correlation exists between the thinning of the cortical layers in PC and the impairment of olfactory capabilities [56]. Inflammation is a common reason for olfactory dysfunction [57,58], while severe inflammation is always found in PD patients [59]; the inflammation environment further inflicts damage on the structure and function of the olfactory epithelium and the OB [60]. In our study, apoptosis and inflammation in the OB and the PC of MPTP-induced subacute PD mice were also found, manifested as the activation of microglia or astrocytes in the OB and PC.…”

Microglial CMPK2 promotes neuroinflammation and brain injury after ischemic stroke

“… 14 Especially, the D-loop bubble of mtDNA is vulnerable to oxidative stress and then is oxidized by ROSs to produce Ox-mtDNA, which can directly activate the NLRP3 inflammasome. Furthermore, microglial Hv1 increases ROS generation through NADPH oxidase regulation and then aggravates neuron death and brain injury after neurological disorders, 61 , 62 , 63 , 64 , 65 which may synergize with CMPK2 to exacerbate neuroinflammation and neuron death after ischemic stroke. Our current study showed that CMPK2 knockdown suppressed new mtDNA synthesis, as determined by EdU staining, inhibited levels of representative mtDNA markers, including D-loop, Cox1 , and CYTB , and disrupted Ox-mtDNA formation, as determined by 8-OHdG immunofluorescence staining in primary mouse microglia upon LPS priming followed by ATP stimulation or OGD conditions in vitro .…”