The authors present a study on the association of PRNP and PRND gene polymorphisms with the occurrence and age at onset of Alzheimer’s disease (AD). DNA from 79 Polish patients with probable AD and 107 healthy control subjects was studied. The PRNP codon 129 homozygosity seemed to be associated with the occurrence of AD: In AD patients, the percentage of Val/Val and Met/Met genotypes was higher than in the control subjects. A significant difference appeared also between early-onset (<70 years) and late-onset (≥70 years) AD patients in the PRND genotypes.

Introduction: The punishing effect of the pandemic outbreak of the disease termed COVID-19 (coronavirus disease-19) caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) impelled the author to gather the facts about the nature of this new pathogen. The aim of this paper was to discuss the mechanisms involved in the pathogenesis of neurological complications during the course of COVID-19. State of the art: Neurological symptoms, such as impairment of taste or smell, headache, nausea and/or altered consciousness, are commonly described in COVID-19 patients, although there are emerging clinical reports of more serious conditions such as acute cerebrovascular accidents, encephalitis and demyelinating disease. Whether these manifestations are the direct consequence of viral invasion of the central nervous system, or are caused by indirect mechanisms, is yet to be established. Studies to date have indicated that neurological lesions found in the brains of COVID-19 patients are a combination of direct cytopathic effects caused by SARS-CoV-2 replication and indirect effects due to hypoxia, excessive cytokine reaction, impaired immune response, and cerebrovascular injury induced by viral infection. Studies are still pending into possible routes of SARS-CoV-2 neuroinvasion encompassing the haematopoietic pathway via the blood-brain barrier and retrograde axonal transport through the cranial nerves. Clinical implications: A thorough understanding of SARS-CoV-2 involvement in neurological complications is still lacking. However, our knowledge about SARS-CoV-2 virulence is rapidly expanding, and that has inclined the author to prepare this comprehensive review in the hope that it will improve understanding about the molecular mechanisms underlying neurological abnormalities associated with COVID-19. Future directions: A future detailed study should explore the diagnostics and disease mechanisms so as to enable the development of better therapeutic strategies to reduce the severity of COVID-19 neurological complications. Introduction: The punishing effect of the pandemic outbreak of the disease termed COVID-19 (coronavirus disease-19) caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) impelled the author to gather the facts about the nature of this new pathogen. The aim of this paper was to discuss the mechanisms involved in the pathogenesis of neurological complications during the course of COVID-19. State of the art: Neurological symptoms, such as impairment of taste or smell, headache, nausea and/or altered consciousness, are commonly described in COVID-19 patients, although there are emerging clinical reports of more serious conditions such as acute cerebrovascular accidents, encephalitis and demyelinating disease. Whether these manifestations are the direct consequence of viral invasion of the central nervous system, or are caused by indirect mechanisms, is yet to be established. Studies to date have indicated that neurological lesions found in the brains of COVID-19 patients are a combination of direct cytopathic effects caused by SARS-CoV-2 replication and indirect effects due to hypoxia, excessive cytokine reaction, impaired immune response, and cerebrovascular injury induced by viral infection. Studies are still pending into possible routes of SARS-CoV-2 neuroinvasion encompassing the haematopoietic pathway via the blood-brain barrier and retrograde axonal transport through the cranial nerves. Clinical implications: A thorough understanding of SARS-CoV-2 involvement in neurological complications is still lacking. However, our knowledge about SARS-CoV-2 virulence is rapidly expanding, and that has inclined the author to prepare this comprehensive review in the hope that it will improve understanding about the molecular mechanisms underlying neurological abnormalities associated with COVID-19. Future directions: A future detailed study should explore the diagnostics and disease mechanisms so as to enable the development of better therapeutic strategies to reduce the severity of COVID-19 neurological complications.

Despite many studies, our knowledge on the impact of antibiotics and antibiotic-resistant bacteria on the metabolic activity of soil microbial communities is still limited. To ascertain this impact, the community level physiological profiles (CLPPs) and the activity of selected enzymes (dehydrogenase, urease, and phosphatases) in soils treated with vancomycin (VA) and/or multidrug resistant Citrobacter freundii were determined during a 90-day experiment. A multivariate analysis and the resistance (RS)/resilience (RL) concept were used to assess the potential of native microorganisms to maintain their catabolic activity under exposure of VA and/or a high level of C. freundii. In addition, the dissipation rate of VA was evaluated in non-sterile (nsS) and sterile (sS) soils. The results revealed a negative impact of VA on the metabolic activity of soil microorganisms on days 1, 15, and 30 as was showed by a decrease in the values of the CLPP indices (10–69%) and the enzyme activities (6–32%) for treated soils as compared to the control. These observations suggested a low initial resistance of soil microorganisms to VA and/or C. freundii but they were resilient in the long term. Considering the mean values of the RS index, the resistance of measured parameters was categorized in the following order: alkaline phosphatase (0.919) > acid phosphatase (0.899) > dehydrogenase (0.853) > the evenness index (0.840) > urease (0.833) > the Shannon-Wiener index (0.735) > substrate richness (0.485) > the AWCD (0.301). The dissipation process of VA was relatively fast and independent of the concentration used. The DT50 values for VA applied at both concentrations were about 16 days. In addition, the dissipation of VA in nsS was three times faster compared to the dissipation of antibiotic in sS. In conclusion, both CLPP and enzyme activities assays appeared to be useful tool for the determination of disturbances within soil microbial communities and used together may be helpful to understand the changes in their catabolic features. The entry of large quantities of VA and/or C. freundii into soil may temporarily change microbial activity thus pose a potential risk for soil functioning.