Oskar Hansson (Sweden)
Lund University
Clinical Sciences Malmö
Dr. Oskar Hansson gained his PhD in neurobiology in 2001 and his M.D. in 2005. He became senior consultant in neurology in 2012 at Skåne University Hospital, Sweden, and full professor of neurology in 2017 at Lund University, Sweden. Oskar Hansson has performed internationally recognized clinical and translational research focusing on the earliest phases of Alzheimer's and Parkinson’s diseases. His landmark study on cerebrospinal fluid biomarkers for Alzheimer’s disease from 2006 (Hansson et al, The Lancet Neurology, 2006) has been instrumental for the implementation of these biomarkers in the clinical work-up of Alzheimer's disease in Sweden and internationally. His work on biomarkers has led to over 350 original peer-reviewed publications. Ten years ago, he started the prospective and longitudinal Swedish BioFINDER study (www.biofinder.se), where the research team focuses on the development of optimized diagnostic algorithms for early diagnosis, and also studies the consequences of different brain pathologies on cognitive, neurologic and psychiatric symptoms in healthy individuals and patients with dementia and parkinsonian disorders. Recently, the BioFINDER team has shown that tau-PET can differentiate Alzheimer’s from other neurodegenerative diseases (Ossenkoppele et al, JAMA, 2018), and that plasma P-tau is a novel promising blood-based biomarker for early detection of Alzheimer’s disease (Janelidze et al, Nature Medicine, 2020; Palmqvist et al, JAMA, 2020, Nature Medicine, 2021). Besides being responsible for the outpatient ward of the Memory Clinic at Skåne University Hospital, he is also in leading positions of several research networks and he is co-director of the strategic research area of neuroscience at Lund University.

Moderator of 1 Session

 Conference Calendar
FORUM

FORUM ON:BLOOD-BASED BIOMARKERS COMPARISON TO FLUID-BASED BIOMARKERS, IMAGING, AND ASSESSMENT OF DIAGNOSTIC & TREATMENT EFFECTS TREATMENT EFFECT: HOW TO MEASURE MINIMAL CLINICAL EFFICACY?

Session Type
FORUM
Date
Wed, 16.03.2022
Session Time
06:30 PM - 07:30 PM
Room
ONSITE PLENARY: 115-117
Chair(s)

Presenter of 2 Presentations

 Conference Calendar

FLUID AND PET IMAGING BIOMARKERS FOR ALZHEIMER’S AND PARKINSON’S DISEASES

Session Name
0280 - PLENARY LECTURE 2: FLUID AND PET IMAGING BIOMARKERS FOR ALZHEIMER’S AND PARKINSON’S DISEASES (ID 12)
Session Type
PLENARY LECTURE
Date
Wed, 16.03.2022
Session Time
12:00 PM - 12:30 PM
Room
ONSITE PLENARY: 115-117
Lecture Time
12:00 PM - 12:30 PM
Presenter

Abstract

Abstract Body

There is need for biomarkers that improve the diagnostic work-up of neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson's disease (PD), which can be used in both clinical practice and trials. In this talk I will focus on recent advances in blood-based biomarkers, and how these can be combined with other easily accessible and low-cost biomarkers to improve detection of early AD. For example, we have recently shown that combining plasma P-tau with brief cognitive tests of memory and executive function can with high accuracy predict future development of AD in patients with subjective cognitive decline or mild cognitive impairment, which outperformed the baseline clinical assessment of dementia experts. Further, I will discuss steps needed to be taken before AD-relevant blood-based biomarkers can be implemented in clinical practice globally. There will also be a discussion on how blood and PET biomarkers can improve clinical trials evaluating disease modifying therapies, when it comes to enrichment of study participants to be included in the trials as well as when measuring relevant effects of the treatments. Finally, I will discuss the potential use of novel seeding aggregation assays for a-synuclein pathology for early detection of Lewy body disease in the context of selecting appropriate participants for clinical trials.

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SUBGROUP ANALYSES OF THE PLASMA P-TAU181 POPULATION FROM EMERGE/ENGAGE, PHASE 3 CLINICAL TRIALS EVALUATING ADUCANUMAB IN EARLY ALZHEIMER’S DISEASE

Session Name
1200 - ABETA TARGETING THERAPIES IN AD 1 (ID 66)
Session Type
SYMPOSIUM
Date
Fri, 18.03.2022
Session Time
02:45 PM - 04:45 PM
Room
ONSITE: 112
Lecture Time
03:15 PM - 03:30 PM
Presenter

Abstract

Aims

We investigated the effect of aducanumab treatment on plasma p-tau181 levels via prespecified subgroup analyses from the Phase 3 trials EMERGE (NCT02484547) and ENGAGE (NCT02477800).

Methods

In the Phase 3 studies of aducanumab, participants were randomized (1:1:1) to receive high-dose aducanumab, low-dose aducanumab, or placebo monthly over 18 months. Plasma samples were obtained from all participants. Plasma p-tau181 levels were assessed in those participants with samples at Baseline and Week 78.

Subgroup analyses of plasma p-tau181 levels were conducted for factors that included age (≤64, 65 to 74, or ≥75 years), sex (male or female), ApoE ε4 status (carrier or noncarrier), baseline clinical stage (MCI due to AD or mild AD dementia) and use of AD symptomatic medications at baseline (yes or no).

Results

A total of 870 participants in EMERGE and 945 participants in ENGAGE were included in this analysis. A reduction in plasma p-tau181 levels in high-dose and low-dose aducanumab groups compared with placebo was observed across subgroups in both EMERGE and ENGAGE. Results were consistent with overall plasma p-tau181 results from the studies, in which aducanumab significantly lowered plasma p-tau181 levels in a dose and time- dependent manner. A greater treatment response with respect to plasma p-tau181 levels was consistently observed in individuals who were ≥75 years old at baseline and in ApoE ε4 noncarriers.

Conclusions

Plasma p-tau181 levels are a biomarker of Alzheimer’s disease pathology. Subgroup analysis revealed a consistent reduction in plasma p-tau181 levels in participants treated with aducanumab across all subgroups investigated.

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