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Medicina (Kaunas) ; 56(12)2020 Nov 25.
Article in English | MEDLINE | ID: covidwho-1024601


BACKGROUND AND OBJECTIVES: Coronavirus disease 2019 (COVID-19) is a highly contagious infectious disease, responsible for a global pandemic that began in January 2020. Human/COVID-19 interactions cause different outcomes ranging from minor health consequences to death. Since social interaction is the default mode by which individuals communicate with their surroundings, different modes of contagion can play a role in determining the long-term consequences for mental health and emotional well-being. We examined some basic aspects of human social interaction, emphasizing some particular features of the emotional contagion. Moreover, we analyzed the main report that described brain damage related to the COVID-19 infection. Indeed, the goal of this review is to suggest a possible explanation for the relationships among emotionally impaired people, brain damage, and COVID-19 infection. RESULTS: COVID-19 can cause several significant neurological disorders and the pandemic has been linked to a rise in people reporting mental health problems, such as depression and anxiety. Neurocognitive symptoms associated with COVID-19 include delirium, both acute and chronic attention and memory impairment related to hippocampal and cortical damage, as well as learning deficits in both adults and children. CONCLUSIONS: Although our knowledge on the biology and long-term clinical outcomes of the COVID-19 infection is largely limited, approaching the pandemic based on lessons learnt from previous outbreaks of infectious diseases and the biology of other coronaviruses will provide a suitable pathway for developing public mental health strategies, which could be positively translated into therapeutic approaches, attempting to improve stress coping responses, thus contributing to alleviate the burden driven by the pandemic.

Brain Diseases/virology , COVID-19 , Mental Health , Psychological Distress , SARS-CoV-2/pathogenicity , Adaptation, Psychological , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/psychology , Humans
Int J Mol Sci ; 21(9)2020 Apr 28.
Article in English | MEDLINE | ID: covidwho-133432


BACKGROUND: On the 31 December 2019, the World Health Organization (WHO) was informed of a cluster of cases of pneumonia of unknown origin detected in Wuhan City, Hubei Province, China. The infection spread first in China and then in the rest of the world, and on the 11th of March, the WHO declared that COVID-19 was a pandemic. Taking into consideration the mortality rate of COVID-19, about 5-7%, and the percentage of positive patients admitted to intensive care units being 9-11%, it should be mandatory to consider and take all necessary measures to contain the COVID-19 infection. Moreover, given the recent evidence in different hospitals suggesting IL-6 and TNF-α inhibitor drugs as a possible therapy for COVID-19, we aimed to highlight that a dietary intervention could be useful to prevent the infection and/or to ameliorate the outcomes during therapy. Considering that the COVID-19 infection can generate a mild or highly acute respiratory syndrome with a consequent release of pro-inflammatory cytokines, including IL-6 and TNF-α, a dietary regimen modification in order to improve the levels of adiponectin could be very useful both to prevent the infection and to take care of patients, improving their outcomes.

Antioxidants/administration & dosage , Betacoronavirus , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Diet , Dietary Supplements , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Adiponectin/metabolism , Ascorbic Acid/administration & dosage , COVID-19 , Coronavirus Infections/metabolism , Fatty Acids, Omega-3/administration & dosage , Fatty Acids, Omega-3/metabolism , Flavonoids/administration & dosage , Humans , Interleukin-6/immunology , Interleukin-6/metabolism , Lung Diseases/immunology , Lung Diseases/metabolism , Lung Diseases/therapy , Pandemics , Pneumonia, Viral/metabolism , SARS-CoV-2 , Tumor Necrosis Factor-alpha/metabolism