ArticleJournal of neuropathology and experimental neurology2017
Disease and Region Specificity of Granulin Immunopositivities in Alzheimer Disease and Frontotemporal Lobar Degeneration.
Article in Journal of neuropathology and experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting Granulin Haploinsufficiency in Frontotemporal Dementia: From Genetic Mechanisms to Therapeutics.International journal of molecular sciences · 2025Review
- Proteomic changes upon treatment with semaglutide in individuals with obesity.Nature medicine · 2025Article
- FAM76B regulates PI3K/Akt/NF-κB-mediated M1 macrophage polarization by influencing the stability of PIK3CD mRNA.Cellular and molecular life sciences : CMLS · 2024Article
- Lycium barbarum polysaccharide alleviates dextran sodium sulfate-induced inflammatory bowel disease by regulating M1/M2 macrophage polarization via the STAT1 and STAT6 pathways.Frontiers in pharmacology · 2023Article
- Neuropathologic Findings in Elderly HIV-Positive Individuals.Journal of neuropathology and experimental neurology · 2022Article
- Charge and redox states modulate granulin-TDP-43 coacervation toward phase separation or aggregation.Biophysical journal · 2022Article
- Cortical and subcortical pathological burden and neuronal loss in an autopsy series of FTLD-TDP-type C.Brain : a journal of neurology · 2022Article
- Microglia regulate brain progranulin levels through the endocytosis/lysosomal pathway.JCI insight · 2021Article
- Differential neuropathology and functional outcome after equivalent traumatic brain injury in aged versus young adult mice.Experimental neurology · 2021Article
- Modeling Brain Pathology of Niemann-Pick Disease Type C Using Patient-Derived Neurons.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology.Advances in experimental medicine and biology · 2021Article
- Granulins modulate liquid-liquid phase separation and aggregation of the prion-like C-terminal domain of the neurodegeneration-associated protein TDP-43.The Journal of biological chemistry · 2020Article
- Characterization of lysosomal proteins Progranulin and Prosaposin and their interactions in Alzheimer's disease and aged brains: increased levels correlate with neuropathology.Acta neuropathologica communications · 2019Article
- FTLD-TDP With and Without GRN Mutations Cause Different Patterns of CA1 Pathology.Journal of neuropathology and experimental neurology · 2019Article
- Microglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response.Frontiers in cellular neuroscience · 2018Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Heterozygous loss-of-function mutations in GRN, the progranulin gene, which result in progranulin (PGRN) protein haploinsufficiency, are a major cause of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP). PGRN is composed of seven and a half repeats of a highly conserved granulin motif that is cleaved to produce the granulin peptides A-G and paragranulin. To better understand the role of PGRN and granulin (Grn) peptides in the pathogenesis of neurodegeneration, we evaluated PGRN/Grn in brains of patients with Alzheimer disease, FTLD-TDP type A with or without GRN mutations, and normal individuals, using a panel of monoclonal antibodies against Grn peptides A-G. In the neocortex, Grn peptide-specific immunostains were observed, for example, membranous Grn E immunopositivity in pyramidal neurons, and Grn C immunopositivity in ramified microglia. In the hippocampus, Grn immunopositivity in the CA1 and CA2 regions showed disease-specific changes in both neurons and microglia. Most interestingly, in FTLD-TDP type A with GRN mutations, there is a 60% decrease in the density of Grn-positive microglia in the hippocampal CA1, suggesting that haploinsufficiency of the GRN mutations also extends to PGRN expression in microglia. This study provides important insights into future studies of the pathogenesis and treatment of FTLD-TDP.
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Registered trials
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