Sara Hall, Sweden

Skåne University Hospital Clinical Memory Research Unit, Memory Clinic
Sara Hall is a postdoc researcher at the Clinical Memory Research Unit, Malmö, Lund University, Sweden in Professor Oskar Hansson´s research group. Her research is focused on diagnostic and prognostic biomarkers in CSF and blood in Parkinsonian disorders, with a special interest in the cognitive aspects of these disorders. She is also a consultant physician at the Memory Clinic, Skane University Hospital, Malmö, Sweden. Sara graduated from Medical School at the Karolinska Institute in Stockholm, Sweden in 2002. During her residency at the Neurology Clinic in Lund, Sweden she was also active in the creation of the Parkinsonian cohort in the prospective, longitudinal Swedish BioFINDER study as part of her graduate studies. In 2017 she obtained her PhD, defending her thesis “Biomarkers in Parkinson’s disease and related disorders, Diagnostic value of biochemical markers, and their relation to disease progression”. The same year she became a specialist in Neurology. In 2017 she received the Bundy Academy Award for Neurology.

Author Of 2 Presentations

PLASMA PHOSPHO-TAU IDENTIFIES ALZHEIMER’S CO-PATHOLOGY IN PATIENTS WITH LEWY BODY DISEASE WITH DEMENTIA

Session Name
Session Type
SYMPOSIUM
Date
13.03.2021, Saturday
Session Time
08:00 - 10:00
Room
On Demand Symposia B
Lecture Time
08:30 - 08:45
Presenter
Session Icon
On-Demand

Abstract

Aims

To investigate whether plasma phospho-tau217 (P-tau217) and phospho-tau181 (P-tau181) can detect Alzheimer’s disease (AD) co-pathology in patients with dementia with Lewy bodies and Parkinson’s disease with dementia (i.e. Lewy body disease with dementia).

Methods

In this cross-sectional study we investigated the plasma levels of P-tau217 and P-tau181 in 35 patients with dementia with Lewy bodies or Parkinson’s disease with dementia, recruited as part of the Swedish BioFINDER2 study. All patients also underwent tau-PET imaging using 18F-RO948, and cerebrospinal fluid (CSF) was analyzed for P-tau217, P-tau181 and β-amyloid42/40 (Aβ42/Aβ40), biomarkers that reliably detect AD pathology in vivo. Abnormal β-amyloid status was defined as CSF Aβ42/Aβ40 <0.752, determined using mixture modeling.

Results

Plasma P-tau217 correlated with plasma P-tau181 (rs=0.68, p<0.001), CSF P-tau217 (rs=0.68, p<0.001) and negatively with CSF Aβ42/Aβ40 (rs=-0.52, p=0.001). Plasma P-tau181 correlated with CSF P-tau181 (rs=0.55, p<0.001). Both plasma P-tau217 and plasma P-tau181 correlated with 18F-RO948 retention in the temporal meta ROI corresponding to Braak stage I-IV (rs=0.57, p<0.001 and rs=0.66, p<0.001, respectively). Additionally, plasma P-tau217 and plasma P-tau181 predicted abnormal tau-PET status in the temporal meta ROI (AUC 0.84 and 0.78, respectively) as well as abnormal CSF β-amyloid status (AUC 0.88 and 0.81, respectively).

Conclusions

Plasma P-tau might be a useful marker for the detection of AD co-pathology in Lewy body disease with dementia, and could be used for stratification of patients in clinical trials. Further studies are needed to determine whether plasma P-tau provides important prognostic information in patients with Lewy body disease.

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Presenter of 2 Presentations

PLASMA PHOSPHO-TAU IDENTIFIES ALZHEIMER’S CO-PATHOLOGY IN PATIENTS WITH LEWY BODY DISEASE WITH DEMENTIA

Session Name
Session Type
SYMPOSIUM
Date
13.03.2021, Saturday
Session Time
08:00 - 10:00
Room
On Demand Symposia B
Lecture Time
08:30 - 08:45
Presenter
Session Icon
On-Demand

Abstract

Aims

To investigate whether plasma phospho-tau217 (P-tau217) and phospho-tau181 (P-tau181) can detect Alzheimer’s disease (AD) co-pathology in patients with dementia with Lewy bodies and Parkinson’s disease with dementia (i.e. Lewy body disease with dementia).

Methods

In this cross-sectional study we investigated the plasma levels of P-tau217 and P-tau181 in 35 patients with dementia with Lewy bodies or Parkinson’s disease with dementia, recruited as part of the Swedish BioFINDER2 study. All patients also underwent tau-PET imaging using 18F-RO948, and cerebrospinal fluid (CSF) was analyzed for P-tau217, P-tau181 and β-amyloid42/40 (Aβ42/Aβ40), biomarkers that reliably detect AD pathology in vivo. Abnormal β-amyloid status was defined as CSF Aβ42/Aβ40 <0.752, determined using mixture modeling.

Results

Plasma P-tau217 correlated with plasma P-tau181 (rs=0.68, p<0.001), CSF P-tau217 (rs=0.68, p<0.001) and negatively with CSF Aβ42/Aβ40 (rs=-0.52, p=0.001). Plasma P-tau181 correlated with CSF P-tau181 (rs=0.55, p<0.001). Both plasma P-tau217 and plasma P-tau181 correlated with 18F-RO948 retention in the temporal meta ROI corresponding to Braak stage I-IV (rs=0.57, p<0.001 and rs=0.66, p<0.001, respectively). Additionally, plasma P-tau217 and plasma P-tau181 predicted abnormal tau-PET status in the temporal meta ROI (AUC 0.84 and 0.78, respectively) as well as abnormal CSF β-amyloid status (AUC 0.88 and 0.81, respectively).

Conclusions

Plasma P-tau might be a useful marker for the detection of AD co-pathology in Lewy body disease with dementia, and could be used for stratification of patients in clinical trials. Further studies are needed to determine whether plasma P-tau provides important prognostic information in patients with Lewy body disease.

Hide