Papers on incident parkinsonism

Who was studied456,862 White UK Biobank participants with genetic data, median 11.8 years

What changedParkinsonism risk was higher with each additional vascular-related condition (subdistribution hazard ratio 1.30)

The catchParticipants without genetic data were excluded, potentially introducing selection bias

Who was studied374,751 UK Biobank participants without neurodegenerative diseases

What changedHigher blood levels of total branched-chain amino acids, leucine, and valine were linked to lower Parkinson’s disease risk

The catchParkinson’s changes before diagnosis may alter amino acid levels, reversing the apparent causal direction

Who was studied890,712 patients with hypertension, against users of non-RAAS blood-pressure drugs

What changedParkinson's disease risk was lower with irbesartan (HR = 0.588) and olmesartan (HR = 0.797) than with non-RAAS blood-pressure drugs

The catchSmoking, socioeconomic position, and education could confound the association; none were adjusted for

Who was studied6,326 adults with depression, against people with depression without slowing

What changedParkinson's diagnosis rates were higher with slowed movement and thinking than without slowing among people with depression (hazard ratio 1.57)

The catchEarly Parkinson's disease could cause the slowing attributed to depression

Who was studied6,415 initially non-diseased participants, up to 30 years

The catchLower sensitivity of health records likely misclassifies some Alzheimer's cases as non-cases

Who was studiedAdults aged 20-74 years, against nonusers

What changedOdds of a first Parkinson or Alzheimer diagnosis were lower in probiotic medication users than nonusers (odds ratio of 0.56)

The catchDifferences in users' health or health care use may have contributed to the association