Journal of neuroinfectious diseases 

About: Journal of neuroinfectious diseases is an academic journal. The journal publishes majorly in the area(s): Encephalitis & Meningitis. It has an ISSN identifier of 2314-7326. It is also open access. Over the lifetime, 173 publications have been published receiving 498 citations.

Neuropathology of Zika Virus Infection

Abstract: Zika virus (ZIKV) is a member of the Flaviviridae family that had been associated only with mild disease prior to the 2015 outbreak in Brazil. A dramatic increase in reported cases of microcephaly and Guillain-Barre syndrome during this time prompted significant research into possible associations with ZIKV and its neurotropic properties. Infection of neural progenitor cells and organoids have been shown to induce apoptosis and dysregulation of growth, and mouse studies have demonstrated viral replication in brain tissue in adults, as well as vertical transmission resulting in embryonic brain abnormalities. Large case series of clinical and radiological findings of congenital ZIKV infection have begun to be published; however, pathology reports have been limited to two case reports and two small case series. Thus far, the findings have largely been restricted to the brain and include diffuse grey and white matter involvement consisting of dystrophic calcifications, gliosis, microglial nodules, neuronophagia, and scattered lymphocytes. Mild chronic villitis was observed in the placental tissue in some cases, and the remaining organs were essentially uninvolved. Larger, systematic studies, including correlation of histological findings with gestational age at the time of maternal infection, will be required to determine the full range of Zika virus-induced abnormalities and to help guide future clinical decision making.

Neurological Manifestations of Bartonellosis in Immunocompetent Patients: A Composite of Reports from 2005-2012

Abstract: In recent years, an increasing number of Bar- tonella species have been identified as zoonotic pathogens, transmitted by animal bites, scratches or by arthropods. Although historically the term bartonellosis was attributed to infections with Bartonella bacilliformis, transmitted by sandflies in the Peruvian Andes, a more inclusive medical use of this term now includes infections caused by any Bartonella sp., anywhere in the world. Potentially, because Bartonella spp. can infect erythrocytes, endothelial cells, and various macrophage-type cells, including brain-derived dendritic cells in vitro, the clinical and pathological man- ifestations of bartonellosis appear to be very diverse. The purpose of this review is to focus attention on neurological bartonellosis cases reported in immunocompetent patients since 2005. Among these patients, disease course has varied substantially in length and severity, including one fatal case of encephalitis in a child. Based upon the evolving literature, a high clinical index of suspicion is warranted.

Protective Effect of Ginger (Zingiber officinale) on Alzheimer's disease Induced in Rats

Abstract: The possible protective effect of Ginger on Alzheimer’s disease induced in rats was investigated. Ninety rats were used as follows: control group, AD protective group using AlCl3, 3rd, 4th, and 5th groups rats were received orally Rivastigmine, Ginger (108 and 216 mg/kg/day) respectively, for two weeks followed by combination of each treatment for another 4 weeks. 6th group is a therapeutic AD group, while 7th, 8th & 9th groups are AD rats treated with the same doses of Rivastigmine and Ginger for 12 weeks. At baseline and after each treatment, behavioral stress tests, Rotarod and T-Maze tests were done. At the end of all experiments rats' brains were dissected and prepared for determination of acetylcholine (Ach), acetycholinesterase (AchE) levels and histopathologic examination. This study indicated that AD-induced rats exhibited reduction in behavior, Rotarod and T-Maze tests, reduction in brain Ach and increase AchE levels. While rats treated with Rivastigmine and Ginger in protective and therapeutic groups exhibited significant improvement in behavior, Rotarod and T-Maze, significant increase in brain Ach and decrease AchE levels. These results were consistent with the histopathological findings and revealed Rivastagmine, and Ginger ameliorates neurodegeneration characters of Alzheimer’s diseases in rats.

MicroRNAs and Malaria - A Dynamic Interaction Still Incompletely Understood.

Abstract: Malaria is a mosquito-borne infectious disease caused by parasitic protozoa of the genus Plasmodium. It remains a major problem affecting humans today, especially children. However, the pathogenesis of malaria, especially severe malaria, remains incompletely understood, hindering our ability to treat this disease. Of recent interest is the role that small, non-coding RNAs play in the progression, pathogenesis of, and resistance to, malaria. Independent studies have now revealed the presence of microRNA (miRNA) in the malaria parasite, vector, and host, though these studies are relatively few. Here, we review these studies, focusing on the roles specific miRNA have in the disease, and how they may be harnessed for therapeutic purposes.

Alzheimers Disease: A Novel Hypothesis Integrating Spirochetes, Biofilm, and the Immune System

Abstract: In the light of recent studies showing the presence of spirochetes in the brains of Alzheimer’s disease (AD) patients, we have studied (post mortem) the hippocampus region in the brains of similarly affected AD patients utilizing both pathology and immunohistochemistry. Our findings demonstrate that the plaques, which are characteristically found in AD brains, reveal the presence of biofilms. These biofilms are undoubtedly made by the spirochetes present there; further, we have also found that the biofilms co-localize with the β amyloid that is a signature finding in the disease. Also, we have shown activation of Toll-like receptor 2 in the same areas. We postulate this is related to the disease because this innate immune system molecule cannot penetrate the biofilm to destroy the spirochetes present there, so, inasmuch as it is activated, it destroys the surrounding tissue instead. We compare this destruction to that which is caused by activation of the adaptive immune system, which leads to much more severe devastation, much more rapidly.