Sökning: "Prion"

Visar resultat 11 - 15 av 55 avhandlingar innehållade ordet Prion.

1. 11. Prion processing and propagation in neuronal and dendritic cell culture models

   Författare :Katarina M Luhr; Karolinska Institutet; Karolinska Institutet; []
   Nyckelord :Prion; scrapie; cathepsin; processing; IFN-gamma; DRG; dendritic cell; cytokine;

   Sammanfattning : Prion diseases are rare neurodegenerative diseases, associated with a conversion of a normal cellular protein, PrPC, into its misfolded and partial protease resistant isoform, PrPSc. These diseases affect both animals and humans and are unique since they can not only be genetic and sporadic, but also transmissible. LÄS MER

3. 12. Altered cell signaling linked to neurodegeneration : Studies on scrapie-infected neuroblastoma cells and activated microglia

   Författare :Christina Svensson; Tiit Land; Gianluigi Forloni; Stockholms universitet; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Prion disease; Inflammation; MAPK; Microglia activation; Neuroblastoma; Neurochemistry; Neurokemi; Neurochemistry and Neurotoxicology; neurokemi och neurotoxikologi;

   Sammanfattning : Prion diseases are neurodegenerative disorders that can affect humans and animals. The underlying event is a conformational change of the normal cellular prion protein (PrPC) into an aberrant isoform termed PrP-scrapie (PrPSc). PrPSc is thought to lead to neurodegeneration and activation of glial cells. LÄS MER

4. 13. Protein Misfolding in Human Diseases

   Författare :Karin Almstedt; Per Hammarström; Daniel Otzen; Linköpings universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; Misfolding; carbonic anhydrase; prion protein; protein stability; Biochemistry; Biokemi;

   Sammanfattning : There are several diseases well known that are due to aberrant protein folding. These types of diseases can be divided into three main categories:Loss-of-function diseasesGain-of-toxic-function diseasesInfectious misfolding diseases Most loss-of-function diseases are caused by aberrant folding of important proteins. LÄS MER

5. 14. Neuroinflammation and amyloid-β in early Alzheimer’s disease. Insight into the earliest events using mouse models

   Författare :Megg Gonzales Garcia; Neuroinflammation; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer s disease; amyloid-beta; neuroinflammation; microglia; synapses; prion-like;

   Sammanfattning : Alzheimer’s disease (AD) is the leading cause of dementia and most common neurodegenerative disease worldwide, but there currently exists no effective treatment that can stop nor slow the progression of the disease. The current dogma in the field postulates that the appearance of extracellular amyloid-beta (Aβ) plaques, a histopathological hallmark of the disease, is the trigger for downstream, detrimental events, including neuronal loss, extensive neuroinflammation and cognitive decline. LÄS MER

7. 15. Pulling Force Studies of Secretory Protein Translocation into the Endoplasmic Reticulum

   Författare :Theresa Kriegler; Tara Hessa; Patricia Clark; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; Co-translational translocation; Xbp1 arrest peptide; Translocon-associated protein TRAP complex; Prion protein; Insulin; Biochemistry; biokemi;

   Sammanfattning : More than 30% of human genes encode secretory or membrane proteins. Most secretory proteins are targeted to the Endoplasmic reticulum (ER) membrane via cleavable N-terminal signal sequences either in a co- or post-translational manner. They enter or cross the membrane using a protein translocating channel (translocon). LÄS MER