Aged Grn −/− mouse brains accumulate lysosomal proteins and markers of neuroinflammation Because GO and network analysis revealed that dysregulation of the lysosomal pathway was an early and highly significant event in the Grn −/− mouse brain proteome, we focused on validating and examining these changes using biochemical and immunological orthogonal approaches.
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Network analysis of the progranulin-deficient mouse brain proteome reveals pathogenic mechanisms shared in human frontotemporal dementia caused by GRN mutations.
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