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Stomrud, E.

Publications and source records attributed to Stomrud, E..

3 recordsLinked to original sources

Personalised Regional Modelling Predicts Tau Progression in the Human Brain

Aggregation of the hyperphosphorylated tau protein is a central driver of Alzheimers disease, and its accumulation exhibits a rich spatio-temporal pattern that unfolds during the course of the disease, sequentially progressing through the brain across axonal connections. It is unclear how this spatio-temporal process is orchestrated - namely, to what extent the spread of pathologic tau is governed by transport between brain regions, local production or both. To address this, we develop a mechanistic model from tau PET data to describe tau dynamics along the Alzheimers disease timeline. Our analysis reveals longitudinal changes in production and transport dynamics on two independent cohorts, with subjects in early stage of the disease exhibiting transport-dominated spread, consistent with an initial spread of pathologic tau seeds, and subjects in late stage disease (Braak stage 3/4 onwards) characterised primarily by local production of tau. Furthermore, we demonstrate that the model can accurately predict subject-specific longitudinal tau accumulation at a regional level, potentially providing a new clinical tool to monitor and classify patient disease progression. TeaserA mechanistic model reveals tau protein dynamics in Alzheimers, showing stage-specific shifts in transport and local production.

neuroscience↗

Cerebrospinal fluid reference proteins increase accuracy and interpretability of biomarkers for brain diseases

Cerebrospinal fluid (CSF) biomarkers reflect brain pathophysiology and are used extensively in translational research as well as in clinical practice for diagnosis of neurological diseases, e.g., Alzheimers disease (AD). However, CSF biomarker concentrations may be influenced by non-disease related mechanisms which vary between individuals, such as CSF production and clearance rates. Here we use a data-driven approach to demonstrate the existence of inter-individual variability in mean CSF protein levels. We show that these non-disease related differences cause many commonly reported CSF biomarkers to be highly correlated, thereby producing misleading results if not accounted for. To adjust for this inter-individual variability, we identified and evaluated high-performing reference proteins which improved the diagnostic accuracy of key CSF AD biomarkers. Our novel reference protein method attenuates the risk for false positive findings, and improves the sensitivity and specificity of CSF biomarkers, with broad implications for both research and clinical practice.

neuroscience↗

Independent information from PET, CSF and plasma biomarkers of tau pathology in Alzheimer's disease

PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimers disease (AD) related demographic, cognitive, genetic and neuroimaging markers. We examined 771 participants with normal cognition, mild cognitive impairment or dementia from BioFINDER-2 (n=400) and ADNI (n=371). All had tau-PET ([18F]RO948 in BioFINDER-2, [18F]flortaucipir in ADNI) and CSF p-tau181 biomarkers available. Plasma p-tau181 and plasma/CSF p-tau217 were available in BioFINDER-2 only. Concordance between PET, CSF and plasma tau biomarkers ranged between 66% and 95%. Across the whole group, ridge regression models showed that increased CSF and plasma p-tau181 and p-tau217 levels were independently of tau PET associated with higher age, and APOE{varepsilon}4-carriership and A{beta}-positivity, while increased tau-PET signal in the temporal cortex was associated with worse cognitive performance and reduced cortical thickness. We conclude that biofluid and neuroimaging markers of tau pathology convey partly independent information, with CSF and plasma p-tau181 and p-tau217 levels being more tightly linked with early markers of AD (especially A{beta} pathology), while tau-PET shows the strongest associations with cognitive and neurodegenerative markers of disease progression.

neuroscience↗