A5043820292- Autophagy in Disease and Therapy
- Alzheimer's disease research and treatments
- Cholinesterase and Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- Endoplasmic Reticulum Stress and Disease
- RNA regulation and disease
- Cannabis and Cannabinoid Research
- Nuclear Receptors and Signaling
- Cellular transport and secretion
- CRISPR and Genetic Engineering
- Lipid metabolism and biosynthesis
- Computational Drug Discovery Methods
Karolinska Institutet
2021-2025
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI)
2023
Abstract A major obstacle in Alzheimer’s disease (AD) research is the lack of predictive and translatable animal models that reflect progression drug efficacy. Transgenic mice overexpressing amyloid precursor protein ( App ) gene manifest non-physiological ectopic expression APP its fragments brain, which not observed AD patients. The knock-in circumvented some these problems, but they do exhibit tau pathology neuronal death. We have generated a rat model, with three familiar mutations...
Alzheimer’s disease (AD) is characterized by impaired protein homeostasis leading to amyloid-β peptide (Aβ) amyloidosis. Amyloid precursor (APP) knock-in mice exhibit robust Aβ pathology, providing possibilities determine its effect on including autophagy. Here we compared human AD postmortem brain tissue with brains from two different types of App mice, NL – F and G exhibiting AD-like pathology. In brains, p62 levels are increased p62-positive staining detected in neurons, potential axonal...
ABSTRACT Alzheimer's disease (AD) pathology is characterized by amyloid beta (Aβ) plaques and dysfunctional autophagy. Aβ generated sequential proteolytic cleavage of precursor protein (APP), the site intracellular APP processing highly debated, which may include autophagosomes. Here, we investigated involvement autophagy, including role ATG9 in trafficking applying RUSH system, allows studying transport fluorescently labeled mCherry‐APP‐EGFP a systematic way, starting from endoplasmic...
Abstract Exit from the endoplasmic reticulum is mediated by Sar1/COPII machinery and a number of accessory factors. How initial steps cargo recruitment upstream are remains unclear, but dihydropyridine FLI-06 inhibits into ER exit sites. Here, we used chemical genetics screening approaches in conjunction with treatment identified membrane proteins YIPF5 GOT1A/B as putative components early export processes. Surprisingly, two homologous GOT1A GOT1B, coded GOLT1A GOLT1B , respectively,...