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Journal of Neuropathology

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Covid19 patient's brains show Alzheimer's like signaling

Author(s): Alison Parker*

COVID-19 patients have multi-system organ failure that affects not just the lungs, but also the cardiovascular, neurological, and other systems. The pleiotropy and complexity of organ system failures complicate COVID-19 patient care and contribute to the pandemic's morbidity and mortality to a large extent. Acute Respiratory Distress Syndrome (ARDS) is the most prevalent symptom of severe COVID-19 infection (ARDS). When SARS-CoV-2 infects lung cells, it causes severe inflammation in the lungs, which leads to respiratory failure. Hypoxia, hypotension, increased inflammatory state, Angiotensin-Converting Enzyme 2 (ACE2) receptor downregulation, endogenous catecholamine adrenergic stimulation, and direct viral-induced myocardial injury are all examples of cardiac symptoms. Patients with underlying cardiovascular illness or comorbidities, such as congestive heart failure, hypertension, diabetes, or pulmonary disease, are also more vulnerable.

A third of COVID-19 patients have neurological symptoms, such as headaches, impaired consciousness, and paresthesia’s, in addition to respiratory and cardiac signs. 8 There have also been reports of brain tissue edema, stroke, neuronal degeneration, and neuronal encephalitis. Diffuse neural inflammatory indicators were discovered in >80% of COVID-19 patient brains in a recent investigation, processes that may contribute to the observed neurological symptoms. Hyposmia and hypogeusia, or the loss of the ability to smell and taste respectively, are two more common signs of SARS-CoV-2 infection. Hyposmia has been documented in early-stage Alzheimer’s disease (AD), 3 and AD type II astrocytosis has been seen in COVID-19 patients’ neuropathology investigations.

The ACE2 receptor, which is extensively expressed in pericytes of the human heart and epithelial cells of the respiratory tract, kidney, intestine, and blood vessels, is believed to be the cause of systemic failure in COVID-19 individuals. Although it is unknown if the SARS-CoV-2 virus directly infects neurons in the brain, ACE2 is expressed in the brain, particularly in the respiratory centre and hypothalamus in the brain stem, the thermal centre, and cortex, making these tissues more sensitive to viral invasion. Inflammatory reactions and oxidative stress in various organs and tissues are the principal effects of SARS-CoV-2 infection. It has recently been discovered that the high neutrophil-to-lymphocyte ratio seen in COVID-19 patients is linked to high levels of reactive oxygen species (ROS) and ROS-induced inflammation.


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