A5035332246- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- S100 Proteins and Annexins
- Neuroscience and Neuropharmacology Research
- Amyotrophic Lateral Sclerosis Research
- Bipolar Disorder and Treatment
- Genetic Syndromes and Imprinting
- Health, Environment, Cognitive Aging
- Parkinson's Disease Mechanisms and Treatments
- Cerebrospinal fluid and hydrocephalus
- Neurological Disease Mechanisms and Treatments
- Calpain Protease Function and Regulation
- Cerebrovascular and genetic disorders
- Functional Brain Connectivity Studies
- Prion Diseases and Protein Misfolding
- Genetic Neurodegenerative Diseases
- Tryptophan and brain disorders
- Epilepsy research and treatment
- Medical Imaging Techniques and Applications
- Electrolyte and hormonal disorders
- Schizophrenia research and treatment
- Neurological diseases and metabolism
- Neurological disorders and treatments
- Signaling Pathways in Disease
- Amyloidosis: Diagnosis, Treatment, Outcomes
The Memory Clinic
2021-2025
Lund University
2021-2025
Skåne University Hospital
2021-2025
ADx NeuroSciences
2021
Ablynx (Belgium)
2021
Eli Lilly (United States)
2021
University of Gothenburg
2015-2020
Sahlgrenska University Hospital
2019
University of Perugia
2015-2016
Plasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability plasma GFAP to detect Alzheimer's disease (AD) pathology in form AD-related amyloid-β (Aβ) conversion AD dementia mild cognitive impairment (MCI) cohort.
Tau is an axonal microtubule-binding protein. pathology in brain and increased tau concentration the cerebrospinal fluid (CSF) are hallmarks of Alzheimer's disease (AD). Most CSF present as fragments. We immunoprecipitated from identified several endogenous peptides ending at amino acid (aa) 123 or 224 using high-resolution mass spectrometry. raised neo-epitope-specific antibodies against fragments specifically aa 224, respectively. With these antibodies, we performed immunohistochemistry on...
Abstract To date, there is no validated fluid biomarker for tau pathology in Alzheimer’s disease, with contradictory results from studies evaluating the correlation between phosphorylated CSF PET imaging. Tau protein subjected to proteolytic processing into fragments before being secreted CSF. A recent study suggested that cleavage after amino acid 368 by asparagine endopeptidase (AEP) upregulated disease. We used immunoprecipitation followed mass spectrometric analyses evaluate presence of...
<h3>Background and Objectives</h3> Phosphorylated tau (p-tau) in CSF is considered an important biomarker Alzheimer disease (AD) has been incorporated recent diagnostic criteria. Several variants exist, including p-tau at threonines 181 (p-tau181), 217 (p-tau217), 231 (p-tau231). However, no studies have compared their performance or association to β-amyloid (Aβ) tau-PET. Understanding which variant use remains yet answered question. We aimed compare the accuracy of p-tau181, p-tau217,...
Recent advances in disease-modifying treatments highlight the need for accurately identifying individuals early Alzheimer's disease (AD) stages and monitoring of treatment effects. Plasma measurements phosphorylated tau (p-tau) are a promising biomarker AD, but different assays show varying diagnostic prognostic accuracies. The objective this study was to determine clinical performance novel plasma p-tau217 (p-tau217) assay, p-tau217+Janssen, perform head-to-head comparison an established...
Injured pericytes in the neurovascular unit release platelet-derived growth factor β (PDGFRβ) into CSF. However, it is not clear how pericyte injury contributes to Alzheimer disease (AD)-related changes and blood-brain barrier (BBB) damage. We aimed test whether CSF PDGFRβ was associated with different AD-associated age-associated pathologic leading dementia.PDGFRβ measured of 771 participants cognitively unimpaired (CU, n = 408), mild cognitive impairment (MCI, 175), dementia (n 188) from...
Abstract The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer’s disease (AD). While strongly associated with amyloid-beta (Aβ), its relationship tau accumulation less understood. Studies evaluating role of on showed conflicting results, particularly regarding independence these associations from Aβ load. In this study, we examined three independent longitudinal cohorts (BioFINDER-1, BioFINDER-2 and WRAP) in which participants had cross-sectional measures tangles...
Studies comparing CSF and PET tau biomarkers have included only commercial assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p) mid-domain (i.e. total tau, T-tau). Moreover, these studies did not examine levels in relation to cerebral glucose metabolism. We thus aimed measures, using both novel assays, [18F]THK5317 (tau) [18F]FDG (glucose metabolism).Fourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent studies, with follow-up...
Frontotemporal dementia (FTD) is a pathologically heterogeneous neurodegenerative disorder associated usually with tau or TDP-43 pathology, although some phenotypes such as logopenic variant primary progressive aphasia are more commonly Alzheimer's disease pathology. Currently, there no biomarkers able to diagnose the underlying pathology during life. In this study, we aimed investigate potential of novel species within cerebrospinal fluid (CSF) for in FTD.
ABSTRACT Background Recent advances now allow detection of brain‐specific proteins in blood, including neurofilament light chain (NfL), a marker axonal pathology, and glial fibrillary acidic protein (GFAP), indicative astrocytic activation. Given the evidence astroglial pathology neuronal dysfunction bipolar disorder, ongoing debates on neuroprogression, we investigated plasma NfL GFAP levels affected individuals. Methods This study analysed measured 216 individuals using Simoa. We used...
Cerebrospinal fluid (CSF) biomarkers have gained increasing importance in the diagnostic work-up of Alzheimer's disease (AD). The core CSF related to AD pathology (Aβ42, t-tau and p-tau) are currently used diagnostics, while candidate markers amyloid metabolism (Aβ38, Aβ40, sAPPα, sAPPβ), synaptic loss (neurogranin), neuroinflammation (YKL-40), neuronal damage (VILIP-1) genetic risk (apolipoprotein E) undergoing evaluation. Diurnal fluctuation concentration has been reported may represent a...
Abstract Background Elevated cerebrospinal fluid (CSF) concentrations of total tau (T-tau) and phosphorylated at Thr181 (P-tau181) protein are typical Alzheimer’s disease (AD). However, the T-tau assay measures only mid-region protein, while in CSF is instead composed a series fragments. One fragment species particular, N-224, shows increased levels AD compared to controls. In this multicentre study, we performed clinical validation N-224 cohorts including patients with subjective cognitive...
Background: Tau aggregation in neurons and glial cells characterizes tauopathies as Alzheimer’s disease (AD), progressive supranuclear palsy (PSP) corticobasal degeneration (CBD). proteolysis has been proposed a trigger for tau fragments have observed brain cerebrospinal fluid (CSF). Our group identified major cleavage at amino acid (aa) 224 CSF; N-terminal ending aa (N-224) were significantly increased AD lacked correlation to total (t-tau) phosphorylated (p-tau) PSP CBD. Objective:...
ABSTRACT Importance Recent methodological developments allow us to measure small amounts of brain-specific proteins in the blood, including neurofilament light chain (NfL), a marker axonal pathology, and glial fibrillary acidic protein (GFAP), astrocytic activation. Given evidence potential astroglial pathology neuronal dysfunction bipolar disorder, these markers may provide further insight into its pathophysiology. Objective We investigated plasma NfL GFAP levels people with depression...
ABSTRACT Objective Timely, accurate distinction between behavioural variant frontotemporal dementia (bvFTD) and primary psychiatric disorders (PPD) is a clinical challenge. Blood biomarkers such as neurofilament light chain (NfL) glial fibrillary acidic protein (GFAP) have shown promise. Prior work has NfL helps distinguish FTD from PPD. Few studies assessed together with GFAP. Methods We investigated plasma GFAP levels in participants bvFTD, bipolar affective disorder (BPAD), major...
Abstract IntroductionPlasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability plasma GFAP to detect Alzheimer’s disease (AD) pathology in form AD-related amyloid-b (Aβ) conversion AD dementia mild cognitive impairment (MCI) cohort.Method160 MCI patients were followed for 4.7 years (average). was defined using cerebrospinal fluid (CSF) Aβ42/40 Aβ42/total tau. Plasma measured at baseline follow-up Simoa...
The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer""s disease (AD). While strongly associated with amyloid-beta (Aβ) accumulation, its relationship tau accumulation less understood. Studies evaluating role of on have shown conflicting results, particularly regarding independence these associations from Aβ load. To clarify relations between APOE4, and tau, we examined three independent longitudinal cohorts (the Swedish BioFINDER-1, BioFINDER-2 WRAP cohorts) in which...
Background: People with a migration background are underrepresented in dementia research and disfavored assessment treatment, many foreign-born individuals remain undiagnosed. Objective: The aim of this study was to examine whether there is inequality the clinical between native Sweden. Methods: Information gathered retrospectively from cohort 91 36 patients attending four memory clinics Skåne, Data included information on cognitive test results, cerebrospinal fluid biomarkers, scores at...
Abstract Background The exploratory NeuroToolKit (Roche Diagnostics International Ltd.) is a panel of automated robust prototype assays measuring cerebrospinal fluid (CSF) Alzheimer’s disease (AD) biomarkers. includes core AD biomarkers Aβ42, Aβ40, p‐tau181 and t‐tau, markers synaptic dysfunction (α‐synuclein neurogranin), astrocytosis (S100b, YKL‐40, glial fibrillary acidic protein [GFAP]), microglial activation inflammation (sTREM2, IL‐6) axonal injury (neurofilament light [NfL]). In this...