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  • Bäckström, David C,M.D.1978-Umeå universitet,Neurovetenskaper,DeDepartment of Neurology, Yale University, New Haven, CT, USA (author)

Prediction and early biomarkers of cognitive decline in Parkinson disease and atypical parkinsonism: a population-based study

  • Article/chapterEnglish2022

Publisher, publication year, extent ...

  • 2022-03-15
  • Oxford University Press (OUP),2022

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/316209
  • https://gup.ub.gu.se/publication/316209URI
  • https://doi.org/10.1093/braincomms/fcac040DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-196241URI

Supplementary language notes

  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Backstrom et al. report that, in a population-based cohort of patients with new-onset Parkinson disease, approximately half develop dementia within 10 years. Measurement of CSF biomarkers together with baseline cognitive function, olfaction and motor disease severity has high accuracy for predicting who will develop dementia. The progression of cognitive decline is heterogeneous in the three most common idiopathic parkinsonian diseases: Parkinson disease, multiple system atrophy and progressive supranuclear palsy. The causes for this heterogeneity are not fully understood, and there are no validated biomarkers that can accurately identify patients who will develop dementia and when. In this population-based, prospective study, comprehensive neuropsychological testing was performed repeatedly in new-onset, idiopathic parkinsonism. Dementia was diagnosed until 10 years and participants (N = 210) were deeply phenotyped by multimodal clinical, biochemical, genetic and brain imaging measures. At baseline, before the start of dopaminergic treatment, mild cognitive impairment was prevalent in 43.4% of the patients with Parkinson disease, 23.1% of the patients with multiple system atrophy and 77.8% of the patients with progressive supranuclear palsy. Longitudinally, all three diseases had a higher incidence of cognitive decline compared with healthy controls, but the types and severity of cognitive dysfunctions differed. In Parkinson disease, psychomotor speed and attention showed signs of improvement after dopaminergic treatment, while no such improvement was seen in other diseases. The 10-year cumulative probability of dementia was 54% in Parkinson disease and 71% in progressive supranuclear palsy, while there were no cases of dementia in multiple system atrophy. An easy-to-use, multivariable model that predicts the risk of dementia in Parkinson disease within 10 years with high accuracy (area under the curve: 0.86, P < 0.001) was developed. The optimized model adds CSF biomarkers to four easily measurable clinical features at baseline (mild cognitive impairment, olfactory function, motor disease severity and age). The model demonstrates a highly variable but predictable risk of dementia in Parkinson disease, e.g. a 9% risk within 10 years in a patient with normal cognition and CSF amyloid-beta(42) in the highest tertile, compared with an 85% risk in a patient with mild cognitive impairment and CSF amyloid-beta(42) in the lowest tertile. Only small or no associations with cognitive decline were found for factors that could be easily modifiable (such as thyroid dysfunction). Risk factors for cognitive decline in multiple system atrophy and progressive supranuclear palsy included signs of systemic inflammation and eye movement abnormalities. The predictive model has high accuracy in Parkinson disease and might be used for the selection of patients into clinical trials or as an aid to improve the prevention of dementia.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Granåsen, Gabriel,PhD,1980-Umeå universitet,Epidemiologi och global hälsa(Swepub:umu)galgrn00 (author)
  • Jakobson Mo, Susanna,Medicine Doktor,1968-Umeå universitet,Diagnostisk radiologi,Umeå centrum för funktionell hjärnavbildning (UFBI)(Swepub:umu)suja0009 (author)
  • Riklund, Katrine,MD, PhD, Professor,1963-Umeå universitet,Diagnostisk radiologi,Umeå centrum för funktionell hjärnavbildning (UFBI)(Swepub:umu)kaah0001 (author)
  • Trupp, MilesUmeå universitet,Neurovetenskaper(Swepub:umu)mitr0006 (author)
  • Zetterberg, Henrik,1973Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease and UCL Queen Square Institute of Neurology, London, UK; UK Dementia Research Institute at UCL, London, UK(Swepub:gu)xzethe (author)
  • Blennow, Kaj,1958Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden(Swepub:gu)xbleka (author)
  • Forsgren, LarsUmeå universitet,Neurovetenskaper(Swepub:umu)lafo0001 (author)
  • Eriksson Domellöf, MagdalenaUmeå universitet,Institutionen för psykologi(Swepub:umu)maaeon98 (author)
  • Umeå universitetNeurovetenskaper (creator_code:org_t)

Related titles

  • In:Brain Communications: Oxford University Press (OUP)4:22632-1297

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