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1. Antisense suppression of glial fibrillary acidic protein as a treatment for Alexander disease Abstract Objective: Alexander disease is a fatal leukodystrophy caused by autosomal dominant gain-of-function mutations in the gene for glial fibrillary acidic protein (GFAP), an intermediate filament protein primarily expressed in astrocytes of the central nervous system. A key feature of pathogenesis is over-expression and accumulation of GFAP, with formation of...
2. Plasma Glial Fibrillary Acidic Protein, Copeptin, and Matrix Metalloproteinase-9 Concentrations among West African Stroke Subjects Compared with Stroke-Free Controls Measurement of plasma molecular markers among stroke patients has been proposed as an avenue for improving the accuracy of stroke diagnosis. There is paucity of data on the potential role of these markers in resource-limited settings, where the burden of stroke is greatest. Read More......
3. Familial human prion diseases associated with prion protein mutations Y226X and G131V are transmissible to transgenic mice expressing human prion protein Human familial prion diseases are associated with mutations at 34 different prion protein (PrP) amino acid residues. However, it is unclear whether infectious prions are found in all cases. Mutant PrP itself m… Read More......
4. D409H GBA1 mutation accelerates the progression of pathology in A53T α-synuclein transgenic mouse model Heterozygous mutations in glucocerebrosidase 1 (GBA1) are a major genetic risk factor for Parkinson’s disease and Dementia with Lewy bodies. Mutations in GBA1 leads to GBA1 enzyme deficiency, and GBA1-associated … Read More......