Publications by authors named "P Kallunki"
Seed amplification assays (SAAs) are a promising avenue for the early diagnosis of neurodegenerative diseases. However, when amplifying fibrils from patient-derived samples in multiwell plates, it is currently highly challenging to accurately quantify the aggregates. It is therefore desirable to transfer such assays into a digital format in microemulsion droplets to enable direct quantification of aggregate numbers.
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- * Background research highlights how Zr-immuno-PET imaging can effectively visualize therapeutic antibodies utilizing transferrin-mediated transport across the blood-brain barrier and emphasizes the significance of alpha-synuclein in diseases like Parkinson’s.
- * The methodology involved conjugating antibodies with a chelator and using various analyses, including radioim
Article Synopsis
- A novel α-synuclein seed amplification assay (synSAA) was developed to differentiate misfolded α-synuclein seeds linked to multiple system atrophy (MSA) and Parkinson's disease (PD).
- The study analyzed cerebrospinal fluid (CSF) and brain samples from various clinical cohorts across multiple medical centers to assess the assay's diagnostic accuracy.
- Findings showed that brain samples with Lewy bodies were positive for synSAA, indicating potential for the assay in distinguishing between MSA and PD in diagnostic settings.
Background: Immunotherapy targeting pathological α-synuclein (α-syn) species is a promising strategy for slowing disease progression in neurodegenerative synucleinopathies, including Parkinson's disease (PD).
Objective: The aim was to evaluate the safety, tolerability, pharmacokinetics, and target engagement of ascending doses of Lu AF82422.
Methods: In this first-in-human study (NCT03611569), healthy participants (18-55 years, cohort A) and patients with PD (40-80 years, Hoehn and Yahr stage ≤3, cohort B) were enrolled in ascending-dose cohorts and randomly assigned to receive single intravenous infusions of Lu AF82422 (cohorts A1-A6: 75, 225, 750, 2250 4500, and 9000 mg, respectively; cohorts B1 and B2: 2250 and 9000 mg, respectively) or placebo.
Corrigendum to: DYRK1A interacts with the REST/NRSF-SWI/SNF chromatin remodelling complex to deregulate gene clusters involved in the neuronal phenotypic traits of Down syndrome.
Hum Mol Genet
June 2022