Affiliation:
1. Departamento de Bioquímica Clínica, Área Hematología, Hospital de Clínicas “José de San Martín”, Universidad
de Buenos Aires, Av. Córdoba 2351, C1120AAF Buenos Aires, Argentina
2. Departamento de Bioquímica
Clínica, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC),
Universidad de Buenos Aires, Córdoba 2351, C1120AAF Buenos Aires, Argentina
Abstract
Abstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized
by marked cognitive decline, memory loss, and spatio-temporal troubles and, in severe
cases, lack of recognition of family members. Neurological symptoms, cognitive disturbances,
and the inflammatory frame due to COVID-19, together with long-term effects,
have fueled renewed interest in AD based on similar damage. COVID-19 also
caused the acceleration of AD symptom onset. In this regard, the morbidity and mortality
of COVID-19 were reported to be increased in patients with AD due to multiple pathological
changes such as excessive expression of the viral receptor angiotensin-converting enzyme
2 (ACE2), comorbidities such as diabetes, hypertension, or drug-drug interactions
in patients receiving polypharmacy and the high presence of proinflammatory molecules.
Furthermore, the release of cytokines, neuroinflammation, oxidative stress, and ferroptosis
in both diseases showed common underlying mechanisms, which together worsen the
clinical picture and prognosis of these patients.
Publisher
Bentham Science Publishers Ltd.
Subject
Pharmacology,Molecular Medicine,Drug Discovery,Biochemistry,Organic Chemistry
Cited by
4 articles.
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