A5075964502- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Functional Brain Connectivity Studies
- Advanced Neuroimaging Techniques and Applications
- Medical Imaging Techniques and Applications
- Neurological Disease Mechanisms and Treatments
- Parkinson's Disease Mechanisms and Treatments
- Advanced MRI Techniques and Applications
- Health, Environment, Cognitive Aging
- Neuroinflammation and Neurodegeneration Mechanisms
- Epilepsy research and treatment
- Cancer-related cognitive impairment studies
- Cerebrovascular and Carotid Artery Diseases
- Neuroscience and Neuropharmacology Research
- S100 Proteins and Annexins
- Bioinformatics and Genomic Networks
- Medical Image Segmentation Techniques
- Radiomics and Machine Learning in Medical Imaging
- Health Systems, Economic Evaluations, Quality of Life
- Lanthanide and Transition Metal Complexes
- Genetic Neurodegenerative Diseases
- Tryptophan and brain disorders
- Computational Drug Discovery Methods
- Cholinesterase and Neurodegenerative Diseases
- Machine Learning in Healthcare
Sahlgrenska University Hospital
2018-2025
University of Gothenburg
2016-2025
University College London
2018-2025
National Hospital for Neurology and Neurosurgery
2018-2025
UK Dementia Research Institute
2019-2025
Region Västra Götaland
2024-2025
Stavanger University Hospital
2023-2025
University of Hohenheim
2025
LMU Klinikum
2025
Ludwig-Maximilians-Universität München
2025
SEE SARAZIN ET AL DOI101093/BRAIN/AWW041 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: The advent of the positron emission tomography tracer (18)F-AV1451 provides unique opportunity to visualize regional distribution tau pathology in living human brain. In this study, we tested hypothesis that is closely linked symptomatology and patterns glucose hypometabolism Alzheimer's disease, contrast more diffuse amyloid-β pathology. We included 20 patients meeting criteria for probable disease...
It is not known exactly where amyloid-β (Aβ) fibrils begin to accumulate in individuals with Alzheimer's disease (AD). Recently, we showed that abnormal levels of Aβ42 cerebrospinal fluid (CSF) can be detected before amyloid using PET preclinical AD. Using these approaches, here identify the earliest AD stage subjects from ADNI and BioFINDER cohorts. We show Aβ accumulation preferentially starts precuneus, medial orbitofrontal, posterior cingulate cortices, i.e., several core regions default...
Abstract The quantification of phosphorylated tau in biofluids, either cerebrospinal fluid (CSF) or plasma, has shown great promise detecting Alzheimer’s disease (AD) pathophysiology. Tau at threonine 231 (p-tau231) is one such biomarker CSF but its usefulness as a blood currently unknown. Here, we developed an ultrasensitive Single molecule array (Simoa) for the plasma p-tau231 which was validated four independent cohorts ( n = 588) different settings, including full AD continuum and non-AD...
Astrocytes colocalize with fibrillar amyloid-β (Aβ) plaques in postmortem Alzheimer disease (AD) brain tissue. It is therefore of great interest to develop a PET tracer for visualizing astrocytes vivo, enabling the study regional distribution both and Aβ. A multitracer investigation was conducted patients mild cognitive impairment (MCI), AD, healthy controls using <sup>11</sup>C-deuterium-L-deprenyl (<sup>11</sup>C-DED) measure monoamine oxidase B located astrocytes. Along <sup>11</sup>C-DED...
Increased cerebrospinal fluid neurofilament light (NfL) is a recognized biomarker for neurodegeneration that can also be assessed in blood. Here, we investigate plasma NfL as marker of 13 neurodegenerative disorders, Down syndrome, depression and cognitively unimpaired controls from two multicenter cohorts: King's College London (n = 805) the Swedish BioFINDER study 1,464). Plasma was significantly increased all cortical amyotrophic lateral sclerosis atypical parkinsonian disorders. We...
<h3>Importance</h3> The positron emission tomography (PET) tracer [<sup>18</sup>F]flortaucipir allows in vivo quantification of paired helical filament tau, a core neuropathological feature Alzheimer disease (AD), but its diagnostic utility is unclear. <h3>Objective</h3> To examine the discriminative accuracy for AD vs non-AD neurodegenerative disorders. <h3>Design, Setting, and Participants</h3> In this cross-sectional study, 719 participants were recruited from 3 dementia centers South...
See Schott and Fox (doi: 10.1093/brain/awv405 ) for a scientific commentary on this article. Alzheimer's disease is multifactorial dementia disorder characterized by early amyloid-β, tau deposition, glial activation neurodegeneration, where the interrelationships between different pathophysiological events are not yet well characterized. In study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic was used to quantify changes in...
Abstract Introduction This study investigated the diagnostic and disease‐monitoring potential of plasma biomarkers in mild cognitive impairment (MCI) Alzheimer's disease (AD) dementia cognitively unimpaired (CU) individuals. Methods Plasma was analyzed using Simoa assays from 99 CU, 107 MCI, 103 AD participants. Results Phosphorylated‐tau181 (P‐tau181), neurofilament light, amyloid‐β (Aβ42/40), Total‐tau Glial fibrillary acidic protein were altered but P‐tau181 significantly outperformed all...
Plasma phosphorylated tau at threonine 181 (p-tau181) has been proposed as an easily accessible biomarker for the detection of Alzheimer disease (AD) pathology, but its ability to monitor progression in AD remains unclear.To study potential longitudinal plasma p-tau181 measures assessing neurodegeneration and cognitive decline comparison neurofilament light chain (NfL), a disease-nonspecific marker neuronal injury.This cohort included data from Alzheimer's Disease Neuroimaging Initiative...
Abstract Tau phosphorylated at threonine 181 (p-tau181) measured in blood plasma has recently been proposed as an accessible, scalable, and highly specific biomarker for Alzheimer’s disease. Longitudinal studies, however, investigating the temporal dynamics of this novel are lacking. It is therefore unclear when disease process p-tau181 increases above physiological levels how it relates to spatiotemporal progression characteristic pathologies. We aimed establish natural time course across...
Alzheimer’s disease (AD) is pathologically characterized by the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles and widespread neuronal loss in brain. In recent years, blood biomarkers have emerged as a realistic prospect to highlight accumulating pathology for secondary prevention trials. Neurofilament light chain (NfL), marker axonal degeneration, robustly elevated many neurological neurodegenerative conditions, including AD. A strong relationship with cerebrospinal fluid...
Abstract In Alzheimer’s disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote spreading. Aβ induces activity, manifesting in increases presynaptic growth-associated protein 43 (GAP-43), which is closely involved plasticity. We therefore tested whether Aβ-related GAP-43 increases, as a marker changes, drive spreading 93 patients across aging spectrum with available CSF GAP-43, amyloid-PET longitudinal tau-PET...
In Alzheimer’s disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration cognitive decline. However, pathophysiological link between Aβ remains unclear, hinders therapeutic efforts to attenuate Aβ-related accumulation. has been found trigger neuronal hyperactivity hyperconnectivity, preclinical research shown that spreads across connected neurons in an activity-dependent manner. Here, we hypothesized hypersynchronicity, resulting...
Abstract INTRODUCTION We assessed the prognostic accuracy of plasma p‐tau217 in predicting progression to mild cognitive impairment (MCI) cognitively unimpaired (CU) individuals over a mean follow‐up 5.65 years after collection (range 1.01–10.47). METHODS included 215 participants from PREVENT−AD cohort with Aβ 42/40 and p‐tau217, 159 cerebrospinal fluid (CSF) 155 18 F‐NAV4694 F‐flortaucipir PET scans. MCI was determined by multidisciplinary consensus among memory experts blind biomarker...