You are presented with a paragraph from a COVID-19 literature. Classify the topics of this piece of text by choosing from the following categories:

- Epidemic Forecasting: The content relates to predictions about the spread of COVID-19.
- Treatment: The paragraph discusses therapeutic methods or medication for COVID-19.
- Prevention: The content covers measures to prevent the spread of COVID-19.
- Mechanism: The paragraph explains the biological mechanisms of the virus.
- Case Report: The content is a report of a COVID-19 case.
- Transmission: The paragraph discusses how COVID-19 is transmitted.
- Diagnosis: The content is about diagnosing COVID-19 in individuals.

Your classification should be provided as an element within a JSON array. The array should be formatted with topics enclosed in double quotes and separated by commas, following the JSON format, for example: ["Topic1", "Topic2", ...]. Include all applicable topics within the array. Your output should be a valid JSON array, and no additional text should be included in your response.

Article:

Increasing evidence suggests that elderly people with dementia are vulnerable to the development of severe coronavirus disease 2019 (COVID-19). In Alzheimer's disease (AD), the major form of dementia, beta-amyloid (Abeta) levels in the blood are increased; however, the impact of elevated Abeta levels on the progression of COVID-19 remains largely unknown. Here, our findings demonstrate that Abeta1-42, but not Abeta1-40, bound to various viral proteins with a preferentially high affinity for the spike protein S1 subunit (S1) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the viral receptor, angiotensin-converting enzyme 2 (ACE2). These bindings were mainly through the C-terminal residues of Abeta1-42. Furthermore, Abeta1-42 strengthened the binding of the S1 of SARS-CoV-2 to ACE2 and increased the viral entry and production of IL-6 in a SARS-CoV-2 pseudovirus infection model. Intriguingly, data from a surrogate mouse model with intravenous inoculation of Abeta1-42 show that the clearance of Abeta1-42 in the blood was dampened in the presence of the extracellular domain of the spike protein trimers of SARS-CoV-2, whose effects can be prevented by a novel anti-Abeta antibody. In conclusion, these findings suggest that the binding of Abeta1-42 to the S1 of SARS-CoV-2 and ACE2 may have a negative impact on the course and severity of SARS-CoV-2 infection. Further investigations are warranted to elucidate the underlying mechanisms and examine whether reducing the level of Abeta1-42 in the blood is beneficial to the fight against COVID-19 and AD.
["Mechanism", "Treatment"]