Complications of stroke can include neuropsychiatric symptoms. However, post-stroke psychosis is rare. We report a case where an acute presentation of psychosis, depression and fluctuating cognitive impairment in a middle-aged man turned out to be related to a silent brain infarction. The patient had a background of poorly controlled type 2 diabetes mellitus with glycated haemoglobin level of 9.0-11.0%, hypertension and ischaemic heart disease. His CT brain results showed multifocal infarct with hypodensities at bilateral lentiform nucleus and bilateral corona radiata. His strong genetic predisposition of psychosis and a history of brief psychotic disorder with complete remission 3 years prior to the current presentation might possibly contribute to his post-stroke atypical neuropsychiatric presentation, and posed diagnostic challenges. He showed marked improvement with risperidone 6 mg nocte, chlorpromazine 50 mg nocte and fluvoxamine of 200 mg nocte. The need of comprehensive treatments to modify his stroke risk factors was addressed.
Leigh syndrome (LS) is one of the most puzzling mitochondrial disorders, which is also known as subacute necrotizing encephalopathy. It has an incidence of 1 in 77,000 live births worldwide with poor prognosis. Currently, there is a poor understanding of the underlying pathophysiological mechanisms of the disease without any available effective treatment. Hence, the inevitability for developing suitable animal and cellular models needed for the development of successful new therapeutic modalities. In this short report, we blocked FOXRED1 gene with small interfering RNA (siRNA) using C57bl/6 mice. Results showed neurobehavioral changes in the injected mice along with parallel degeneration in corpus striatum and sparing of the substantia nigra similar to what happen in Leigh syndrome cases. FOXRED1 blockage could serve as a new animal model for Leigh syndrome due to defective CI, which echoes damage to corpus striatum and affection of the central dopaminergic system in this disease. Further preclinical studies are required to validate this model.
In neurodegenerative diseases, such as Alzheimer's and Parkinson's, microglial cell activation is thought to contribute to their degeneration by producing neurotoxic compounds. While dental pulp stem cells (DPSCs) have been regarded as the next possible cell source for cell replacement therapy (CRT), their actual role when exposed in such harsh environment remains elusive. In this study, the immunomodulatory behavior of DPSCs from human subjects was investigated in a coculture system consisting of neuron and microglia which were treated with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine, which mimics the inflammatory conditions and contribute to degeneration of dopaminergic (DA-ergic) neurons. Assessments were performed on their proliferation, extent of DNA damage, productions of reactive oxygen species (ROS) and nitric oxide (NO), as well as secretion of inflammatory mediators. Notably, DPSCs were shown to attenuate their proliferation, production of ROS, and NO significantly (P