ArticleJournal of neuropathology and experimental neurology2019
FTLD-TDP With and Without GRN Mutations Cause Different Patterns of CA1 Pathology.
Article in Journal of neuropathology and experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- A phosphorylation‑independent monoclonal antibody improves detection of TDP‑43 pathology across frontotemporal lobar degeneration, amyotrophic lateral sclerosis, and limbic predominant age related TDP‑43 encephalopathy neuropathological change.Journal of neuropathology and experimental neurology · 2026Article
- Selective cellular and regional vulnerability in frontotemporal lobar degeneration: a scoping review.Free neuropathology · 2025Review
- Production and characterization of novel monoclonal antibodies against pathological human TDP-43 proteins.Journal of neuropathology and experimental neurology · 2024Article
- Distinct Patterns of Hippocampal Pathology in Alzheimer's Disease with Transactive Response DNA-binding Protein 43.Annals of neurology · 2023Article
- Progranulin and GPNMB: interactions in endo-lysosome function and inflammation in neurodegenerative disease.Journal of neuroinflammation · 2023Review
- Loss of Lysosomal Proteins Progranulin and Prosaposin Associated with Increased Neurofibrillary Tangle Development in Alzheimer Disease.Journal of neuropathology and experimental neurology · 2021Article
- Differential neuropathology and functional outcome after equivalent traumatic brain injury in aged versus young adult mice.Experimental neurology · 2021Article
- NovelNeurology. Genetics · 2021Article
- An update on the rod microglia variant in experimental and clinical brain injury and disease.Brain communications · 2021Review
- Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology.Advances in experimental medicine and biology · 2021Article
- Microglial burden, activation and dystrophy patterns in frontotemporal lobar degeneration.Journal of neuroinflammation · 2020Article
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Authors and funding
12 authors.
Funding
Abstract
Heterozygous loss-of-function mutations in the GRN gene lead to progranulin (PGRN) haploinsufficiency and cause frontotemporal lobar degeneration with TDP-43 pathology type A (FTLD-TDP type A). PGRN is a highly conserved, secreted glycoprotein and functions in the central nervous system as a key modulator of microglial function. Hence, altered microglial function caused by PGRN deficiency may be tied to the pathogenesis of FTLD-TDP. Our previous studies showed that haploinsufficiency of GRN mutations extends to microglial PGRN expression in the hippocampal CA1 region. In this study, we found that the CA1 sector was associated with less neuronal loss and more frequent TDP-43 inclusions in FTLD-TDP type A cases with GRN mutations than in sporadic cases. In addition, the CA1 region in GRN mutation cases contained more rod-like microglia, which also had reduced PGRN expression. These findings suggest that the profile of TDP-43 inclusions, neuronal number, and microgliosis in the CA1 sector of FTLD-TDP type A cases may be influenced by GRN gene expression status.
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