Normally neural involvement in leprosy is an ascending neuritis from the nerve involvement in the dermal lesions. However, in some cases neural involvement is seen in the absence of any dermal lesions. In some of these pure neuritic cases, dermal lesions appear sometime later. It is, therefore, more appropriate to designate such cases as 'primary neuritic' cases. This study is aimed at diagnosing primary neuritic leprosy among patients presenting with only neuritic symptoms. An attempt is also made to classify primary neuritic leprosy on a clinical and histopathological basis. During the period 1979-80, 30 patients reported to the out patient department of Schieffelin Leprosy Research and Training Centre, Karigiri with complaints of neuritic origin. In addition to clinical examination and routine skin smears, investigations such as skin, nerve and nasal biopsies, nerve conduction velocity and lepromin testing were carried out where feasible. 17 of these patients were diagnosed as primary neuritic leprosy and in 7 patients other neurological conditions were diagnosed. The remaining 6 patients were kept under observation and have not shown evidence of leprosy during a two year period of following-up. It is interesting that 4 of the 17 primary neuritic cases developed patches during follow-up period of two years. In the final analysis 7 patients (41.2%) were classified into the lepromatous group and 10 patients (58.8%) in the non-lepromatous group (Table-6). This classification will have a bearing on duration of treatment and for their subsequent release from control.
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Lysophosphatidylinositol (LPI) is an endogenous signaling molecule for the GPR55 receptor. Previous studies have shown that arachidonoyl-lysophosphatidylinositol (LPI-20:4) produced an increase in the inflammatory mediators NLPR3 (inflammasome - 3 marker) and IL-1b in neurons from both rat dorsal root ganglion (DRG) and hippocampal cultures. Because LPI is comprised of a family of lipid structures that vary in fatty acyl composition, the current work examined neuroinflammatory responses to various LPI structures in DRG and hippocampal cultures as assessed by high content fluorescent imaging.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
Department of Spinal Surgery, The Third Affiliated Hospital of Soochow University, Changzhou 213000, Jiangsu, People's Republic of China. Electronic address:
After spinal cord injury (SCI), reactive astrocytes in the injured area are triggered after spinal cord injury (SCI) and to polarize into A1 astrocytes with a proinflammatory phenotype or A2 astrocytes with an anti-inflammatory phenotype. Monopolar spindle binder 2 (MOB2) induces astrocyte stellation, maintains cell homeostasis, and promotes neurite outgrowth; however, its role in the phenotypic transformation of reactive astrocytes remains unclear. Here, we confirmed for the first time that MOB2 is associated with A1/A2 phenotypic switching in reactive astrocytes following SCI in mice.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Hale Building for Transformative Medicine, Room 10006, 60 Fenwood Road, Boston, MA, 02115, USA.
α-Synuclein (αS) is a 140 amino-acid neuronal protein highly enriched in presynaptic nerve terminals. Its progressive accumulation in Lewy bodies and neurites is the hallmark of Parkinson's disease (PD). A growing number of studies highlights a critical interplay between lipid metabolism and αS biology.
View Article and Find Full Text PDFBrain
January 2025
Comprehensive Epilepsy Program, Department of Neurology, University of Virginia, Charlottesville, Virginia 22908, USA.
Seizures in people with dementia (PWD) are associated with faster cognitive decline and worse clinical outcomes. However, the relationship between ongoing seizure activity and postmortem neuropathology in PWD remains unexplored. We compared post-mortem findings in PWD with active, remote, and no seizures using multicentre data from 39 Alzheimer's Disease Centres from 2005 to 2021.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
College of Veterinary Medicine, Konkuk University, 120, Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address:
Rett syndrome (RTT) is a neurological disorder caused by a mutation in the X-linked methyl-CpG binding protein 2 (MECP2), leading to cognitive and motor skill regression. Therapeutic strategies aimed at increasing brain-derived neurotrophic factor (BDNF) levels have been reported; however, BDNF treatment has limitations, including the inability to penetrate the blood-brain barrier, a short half-life, and potential for adverse effects when administered via intrathecal injection, necessitating novel therapeutic approaches. In this study, we focused on the adenosine A receptor (AR), which modulates BDNF and its downstream pathways, and investigated the therapeutic potential of CGS21680, an AR agonist, through in vitro and in vivo studies using R106W RTT model.
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