Epidemiological evidence that Alzheimer's and Parkinson's could be caused by viral infections

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Epidemiological evidence that Alzheimer's and Parkinson's could be caused by viral infections
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Epidemiological evidence that Alzheimer's and Parkinson's could be caused by viral infections Brain Coronavirus Dementia Encephalitis EpsteinBarr Virus Genotyping Influenza Neurodegeneration Parkinsons Alzheimers NeuroCellPress

By Dr. Priyom Bose, Ph.D.Jan 23 2023Reviewed by Danielle Ellis, B.Sc. Several studies have indicated that microbial or viral infection could lead to neurodegenerative disease.

About the Study The current study obtained relevant data from the FinnGen project and the UK Biobank to investigate the potential link between viral exposure and the incidence of various NDDs, such as amyotrophic lateral sclerosis , Alzheimer’s disease , vascular dementia , multiple sclerosis , Parkinson’s disease , and generalized dementia .

Viral encephalitis caused by the varicella-zoster virus was also associated with the manifestation of more than one NDD. An association between herpes simplex virus encephalitis and incidence of AD, genital warts and dementia, hepatitis and AD, EBV and MS, EBV and dementia, and HSV and MS were also found in this study.

Immunology eBook Compilation of the top interviews, articles, and news in the last year. Download a free copy Effective vaccines are available for several viral infections, such as influenza, varicella-zoster , and pneumonia. Even though many of the vaccines, such as the COVID-19 vaccine, do not prevent the occurrence of the disease, they reduce disease severity. Importantly, several studies have provided evidence that vaccination significantly reduces the risk of developing NDD.

Study Limitations The current study has some limitations, including access to only the summary data level of FinnGen. In addition, the authors only had access to cross-sectional and prevalent disease data in UKB. This limitation in data access can cause some noise in data analysis. Also, both the national cohorts used diagnoses based on medical billing codes and not bloodwork or assays conducted in laboratories.

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Walking pace, handgrip strength, age, APOE genotypes, and new-onset dementia: the UK Biobank prospective cohort study - Alzheimer's Research & TherapyWalking pace, handgrip strength, age, APOE genotypes, and new-onset dementia: the UK Biobank prospective cohort study - Alzheimer's Research & TherapyBackground The independent and additive associations of walking pace and grip strength on dementia risk and the potential modifying effects of age, APOE phenotypes, and other dementia risk factors on the walking pace and dementia relationships demand further clarification. We aimed to investigate the independent and additive relationships of walking pace and handgrip strength on the risk of new-onset dementia and examine the potentially modifying effects of age, APOE phenotypes, lifestyle factors, and family history of dementia in the relationships. Methods A total of 495,700 participants from the UK Biobank, who were free of dementia at baseline, were included in this study. Walking pace was self-defined as slow, average, or brisk. Handgrip strength was assessed by dynamometer and was divided into sex-specific quartiles. The APOE genotypes were determined by a combination variant of rs429358 and rs7412. Other dementia risk factors, including education, physical activity, hypertension, depression, diabetes, and family history of dementia, were also collected. The primary outcome was new-onset all-cause dementia. Results Over a median follow-up duration of 12.0 years, 3986 (0.8%) participants developed new-onset all-cause dementia. Compared with those with slow walking pace, participants with average (HR, 0.61; 95%CI: 0.55–0.68) or brisk (HR, 0.59; 95%CI: 0.52–0.67) walking pace had a significantly lower risk of new-onset all-cause dementia. Moreover, compared with those with both slow walking pace and lower handgrip strength (the first quartile), the lowest risk of new-onset all-cause dementia was observed in participants with both average or brisk walking pace and higher handgrip strength (the 2–4 quartiles) (HR, 0.45; 95%CI: 0.40–0.52). Notably, the negative relationship between walking pace and the risk of new-onset all-cause dementia was significantly reduced as APOE ε4 dosage increased (APOE ε4 dosages = 0 or 1: brisk vs. slow: HR, 0.55; 95%CI: 0.48–0.63; vs. A
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