Publications by authors named "S Flunkert"

Background: Parkinson's disease (PD) is a debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons and the accumulation of α-synuclein (α-syn) aggregates. The A53T missense point mutation occurs in autosomal dominant familial PD and has been found to promote the aggregation of α-syn. To investigate the role of the A53T mutation in PD, researchers have developed various mouse models with this mutation.

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Objectives: Aggregation and misfolding of amyloid beta (Aβ) and tau proteins, suggested to arise from post-translational modification processes, are thought to be the main cause of Alzheimer's disease (AD). Additionally, a plethora of evidence exists that links metabolic dysfunctions such as obesity, type 2 diabetes (T2D), and dyslipidemia to the pathogenesis of AD. We thus investigated the combinatory effect of T2D and human glutaminyl cyclase activity (pyroglutamylation), on the pathology of AD and whether astaxanthin (ASX) treatment ameliorates accompanying pathophysiological manifestations.

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Article Synopsis
  • Defective clearance of amyloid-β (Aβ) and inflammation contribute significantly to Alzheimer's disease (AD), with problems in transporting Aβ across the blood-brain barrier leading to plaque formation.
  • A study using porcine brain cells and murine hippocampal cultures showed that the antioxidant astaxanthin (ASX) improved the clearance of misfolded proteins and altered Aβ processing by promoting autophagy and enhancing specific transporters.
  • ASX also demonstrated anti-inflammatory properties by decreasing inflammatory cytokines and shifting microglial cells from a pro-inflammatory state (M1) to a protective state (M2), suggesting its potential as a treatment for AD-related issues.
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Introduction: Autism spectrum disorder (ASD) is a persistent neurodevelopmental condition characterized by two core behavioral symptoms: impaired social communication and interaction, as well as stereotypic, repetitive behavior. No distinct cause of ASD is known so far; however, excitatory/inhibitory imbalance and a disturbed serotoninergic transmission have been identified as prominent candidates responsible for ASD etiology.

Methods: The GABA receptor agonist R-Baclofen and the selective agonist for the 5HT serotonin receptor LP-211 have been reported to correct social deficits and repetitive behaviors in mouse models of ASD.

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