Creutzfeldt-Jakob's disease or Prion Disease or Mad Cow ... - iSites

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Deposition of fibrillar proteinacious material in Creutzfeldt-Jakob’s disease (prion disease) Prion disease: Alteration in the prion protein lead to both intracellular and extracellular accumulation of amyloid aggregates, plaques, similar to those characteristic of AD, and positive to prion protein staining. Probably, replication and accumulation of the protease insensitive PrP sc results in fibril formation and plaque deposition. Alzheimer’s Creutzfeldt-Jakob’s Aguzzi A, Haass C. Science. 2003 Oct 31;302(5646):814-8. Review.
Epidemiology of Creutzfeldt-Jakob’s disease (CJD) CJD is, among the Transmissible Spongiform Encephalopathies, the most diffuse one. CJD can be classified as Sporadic sCJD: etiology not known, caused by both exogenous and endogenous factors, represents 85% of all the cases of CJD. In the United States, there are approximately 200 sporadic CJD cases per year. Familial fCJD: caused by mutations in the gene for PrP (prion protein). 15% of CJD cases are inherited. Iatrogenic iCJD: caused by the spreading of the infectious agent due to contaminated surgical tools, to the transplantation of tissues, or to the administration of pituitary hormones from deceased patients affected by the disease. 1% of CJD cases. Variant vCJD: caused by the transmission of Bovine Spongiform Encephalopathy (BSE) prion to humans (aka Mad Cow disease).
Page 1 and 2: Creutzfeldt-Jakob’s disease or Pr
Page 3 and 4: Severe Brain Atrophy in CDJ’s pat
Page 5 and 6: Models for conformational conversio
Page 7 and 8: Symptoms in Creutzfeldt-Jakob’s D
Page 9 and 10: Cow affected by Bovine Spongiform E
Page 11 and 12: Absence of Protease-K-digested PrP
Page 13: *Neuronal death *Neuronal apoptosis
Page 17 and 18: Incidence of vCJD reported worldwid
Page 19 and 20: Functional domains of the prion pro
Page 21 and 22: Amyloid plaques in TSE Kuru disease
Page 23 and 24: Physiologic role of PrP c Caughey
Page 25 and 26: Infarcts are larger in PrP c KO mic
Page 27 and 28: PrP c protects against oxidative st
Page 29 and 30: PrP c maintains synaptic architectu
Page 31 and 32: PrP c physiological functions
Page 33 and 34: Mechanism of replication of PrP Sc
Page 35 and 36: The “unfortunate” goal of CDJ d
Page 37 and 38: Different biochemical and structura
Page 39 and 40: Fibrils of prion protein: self prop
Page 41 and 42: PMCA: protein misfolding cyclic amp
Page 43 and 44: Inoculation of synthetic strains of
Page 45 and 46: PrP c localizes at the plasma membr
Page 47 and 48: Where does the conversion from PrP
Page 49 and 50: Prion protein scrapie accumulation
Page 51 and 52: Post-translational modifications on
Page 53 and 54: Inhibition of GPI-anchor could redu
Page 55 and 56: PrP aggregates can be found at an i
Page 57 and 58: Induced intracellular aggregates ca
Page 59 and 60: Direct transfer of prion cytosolic
Page 61 and 62: PrP c KO mice are viable, develop n
Page 63 and 64: Accumulation of degenerating lysoso
Page 65 and 66:
Autophagic vacuoles form at the syn
Page 67 and 68:
Autophagy-inducing drugs can regula
Page 69 and 70:
Autophagy as an approach to reduce
Page 71:
Approaches for the treatment of CJD
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