Publications by authors named "Daniel Beis"

Article Synopsis
  • Alzheimer's disease (AD) is a neurodegenerative disorder primarily caused by the toxic effects of amyloid-β (Aβ), making understanding therapies critical.
  • 4-Phenylbutyric acid (4-PBA) shows promise in reducing Aβ toxicity, potentially functioning as a chemical chaperone or inhibiting histone deacetylases (HDACs).
  • In a study using the nematode Caenorhabditis elegans, 4-PBA improved movement and diminished Aβ aggregation, with findings suggesting that its effectiveness relies on activating a heat shock response via HSF-1 while inhibiting HDA-1.
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Article Synopsis
  • Computer-based analysis assessed motility in transgenic GMC101 nematodes expressing human amyloid-β (Aβ) to evaluate the impact of caprylic acid (CA) on proteotoxicity and Aβ aggregation.
  • CA enhanced nematode motility and reduced Aβ aggregation, with gene knockdowns showing that β-oxidation of fatty acids is critical for CA's effectiveness, while other metabolic pathways were not as affected.
  • The positive effects of CA were linked to improved mitochondrial function, highlighting its potential as an alternative energy source in conditions like Alzheimer’s disease where glucose metabolism is impaired.
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The nematode Caenorhabditis elegans is a widely used research model for the investigation of metabolism, aging and age-associated diseases. However, when investigating the impact of natural compounds or drugs on those topics, a major confounder is the metabolism of these test substances by live E. coli bacteria, the standard food source of C.

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Objective: Acute stress induces redistribution of circulating leucocytes in humans. Although effects on lymphocytes as adaptive immune cells are well understood, the mechanisms underlying stress effects on granulocytes and monocytes as innate immune blood cells are still elusive. We investigated whether the stress hormone norepinephrine (NE) and α-adrenergic receptors (α-ADRs) may play a mediating role.

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Background: Serotonin (5-hydroxytryptamine, 5-HT) is a key modulatory neurotransmitter in the mammalian central nervous system (CNS) that plays an important role as a developmental signal. Several lines of evidence associate altered 5-HT signaling with psychopathology in humans, particularly neurodevelopmental disorders such as autism spectrum disorders (ASD). ASD are characterized by persistent social and communication deficits along with stereotyped and repetitive patterns of behavior, with all symptoms emerging early during development.

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Tryptophan hydroxylase (TPH) is a rate limiting enzyme in the synthesis of serotonin (5-HT), a monoamine which works as an autacoid in the periphery and as a neurotransmitter in the central nervous system. In 2003 we have discovered the existence of a second Tph gene, which is expressed exclusively in the brain, and, therefore, is responsible for the 5-HT synthesis in the central nervous system. In the following years several research groups have independently generated Tph2-deficient mice.

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Polymorphisms in the TPH2 gene coding for the serotonin synthesizing enzyme in the brain are considered as risk factors associated with depression and anxiety in humans. However, whether a certain variation in the TPH2 gene leads to decreased brain serotonin production and development of psychological abnormalities remains unresolved. We generated a new mouse model, carrying one Tph2-null allele and one Tph21473G-allele, coding for a hypoactive form of the enzyme.

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Voluntary wheel running has long been known to induce precursor cell proliferation in adult hippocampal neurogenesis in rodents. However, mechanisms that couple activity with the promitotic effect are not yet fully understood. Using tryptophan hydroxylase (TPH) 2 deficient (Tph2-deficient) mice that lack brain serotonin, we explored the relationship between serotonin signaling and exercise-induced neurogenesis.

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Non-selective classical transient receptor potential (TRPC) cation channels share important roles in processes of neuronal development and function. To test the influence of TRPC6 activity on behavior, we developed a TRPC6-deficient (TRPC6(-/-)) mouse model in a BALB/c genetic background. Both, TRPC6(-/-) and wild-type (WT) mice were analyzed first for their general health and reflex status (modified SHIRPA protocol) and then in three different behavioral tests (marble-burying test, square open field and elevated star maze).

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