Does COVID increase the risk of Alzheimer’s disease?

Scientists discover that even mild COVID-19 brain proteins can change that are linked to Alzheimer’s disease, which increases the risk of dementia, which makes urgent problems with public health.

Study: Plasma Proteomic evidence for raised β-amyloid pathology after SARS-COV-2 infection. Image Credit: Ink Drop / Shutterstock

A recent study published in the magazine Nature Medicine Investigated whether both mild and serious cases of severe acute breathing syndrome Coronavirus 2 (SARS-COV-2) infection are linked to changes in brain biomarkers associated with Alzheimer’s disease.

By analyzing blood samples of the participants in the Biobank of the United Kingdom (VK), the researchers discovered that individuals who had COVID-19 showed signs of increased brain pathology, increasing critical problems on public health.

Background

While the world continues to recover from the COVID-19 Pandemie, scientists are investigating their long-term effects on the health of the brain. The past has shown that viral infections can cause systemic inflammation, a key factor in neurodegenerative diseases such as Alzheimer’s disease. Up to evidence suggests that people who have had serious COVID-19 can run a higher risk of cognitive decline, but the underlying mechanisms remain unclear.

Alzheimer’s disease is associated with changes in brain proteins such as beta-amyloid and Tau, which can be detected in blood samples years before disease symptoms appear. Biomarkers such as amyloid-beta ratio (Aβ42: Aβ40), fosphorylored Tau (PTAU-181) and Neuroilament Light chain (NFL) help researchers to assess early signs of neurodegeneration.

Previous studies, however, have focused primarily on serious COVID-19 cases, leaving a gap in understanding the risks for people with mild to moderate infections. In view of the emerging evidence that even mild or moderate cases of COVID-19 can result in post-acute consequences of COVID-19 (PACC), this study was intended to determine whether SARS-COV-2 infection-deachted without Ernstkan Contribute to changes in these critical biomarkers.

About the study

In order to explore the potential link between COVID-19 and the disease-related pathology of Alzheimer’s, the research team analyzed Blood Plasmamonsters from participants in the British Biobank Covid-19-19 Imaging Revestion study.

The study included 626 people who had tested positively on SARS-COV-2 and 626 matched checks that were not infected, which were selected on the basis of health files, antigen test results and antibody tests. The operating elements were coordinated on the basis of age, gender, ethnicity and location to minimize confusing factors. In particular, the study was responsible for important variables such as Apoe genotype, hypertension and lifestyle factors, which caused a more rigorous comparison between cases and controls.

Blood samples were collected before and after the pandemic for the British Biobank study, so that researchers could follow changes in important neurodegeneration -biomarkers. With the help of ultras-sensitive tests, they sizes beta-amyloid (Aβ40, Aβ42), PTAU-181, NFL and Glial fibrillary acid protein (GFAP). In addition, the study used proteomic analysis of 1,468 proteins using the Olink Explore platform, making a broader insight into how SARS-COV-2 influences systemic health.

A, experimental design. Protein concentrations were tested from plasma samples obtained from the British biobank imaging assessment visits, the second of which was specifically recruited for the study of COVID-19. B, distribution of participants ages in the pandemic assessment. C, sources of evidence for case selection. Antibody, home-based lateral SARS-COV-2 antibody test; Antigen, PCR Antigeen (Swab) test; Health files, general practitioners and/or hospital data. D, Distribution of pre-Pandemic Assessment Visit Dates. E, distribution of pandemic assessment visit dates. F, distribution of intervals between reviews. G, estimated dates of COVID symptoms (of participants with antigeent test results). Figure made with biorender.com.

The team also investigated cognitive function and neuroimaging data to assess brain health over time. The study checked for existing conditions such as hypertension, diabetes and obesity to isolate the effect of COVID-19. By comparing the biomark levels before and after the SARS-COV-2 infection, the researchers wanted to determine whether COVID-19 had a measurable impact on early indicators of Alzheimer’s disease.

Findings

The study showed that people with COVID-19 showed significant changes in brain biomarkers associated with Alzheimer’s disease. The Aβ42: Aβ40 ratio, an important marker of beta-amyloid structure, was lower with COVID-19-PROSCIETTER participants compared to their matched controls. A reduced ratio of these proteins is often linked to Alzheimer’s pathology.

In addition, the study increased levels of PTAU-181, a protein associated with tau tanges in the brain, and increased NFL levels, which indicated neuronal damage. Gfap, a marker for astrocyte activation and neuro inflammation, was also higher with those who had Covid-19.

It was striking that these biomarker changes were comparable to four years of aging or 60% of the effect size of inheriting a single apoe-ε4-allel, a well-known genetic risk factor for Alzheimer’s disease.

These changes in the biomarker were more pronounced in older people (in particular those older than 70) and those with existing risk factors such as hypertension and obesity. It is interesting that even participants who had mild or asymptomatic COVID-19 showed changes in their plasma car markers, suggesting that the impact of the infection on brain health may not be limited to serious cases.

The researchers also analyzed cognitive test scores and neuroimaging data and discovered that COVID-19-positive individuals showed lower cognitive test performance compared to controls similar to almost two years of former-related cognitive decline. Brain image formation revealed structural patterns associated with Alzheimer’s disease in some participants, which further strengthens the potential connection between COVID-19 and Neurodegeneration.

Moreover, the study showed that certain inflammatory markers, including TNFSF10 (Trail), PTX3 and IL-6, were changed with post-known people, which suggests a long-term inflammatory reaction that could contribute to brain pathology.

The researchers explained that although this study does not make a direct causal link between COVID-19 and Alzheimer’s, the results are concerned about the potential neurological consequences in the long term of the viral infection. The findings also emphasized the importance of monitoring brain health in patients after the COVID-19 and the consideration of preventive strategies for risk patients.

Conclusions

In general, the study resulted in new evidence that COVID-19 Alzheimer’s can accelerate disease-related brain changes, even in people with mild infections. The observed changes in Plasmabiomarkers suggested a potential long -term impact on the health of the brain.

Although further research is needed to confirm these findings, the authors emphasized that their results correspond to earlier reports that suggest an increased incidence of dementia after COVID-19. These findings emphasize the importance of long-term monitoring, preventive interventions and future public health strategies aimed at reducing post-known neurological risks.