ArticleBiochemical pharmacology2015
Reducing inflammation and rescuing FTD-related behavioral deficits in progranulin-deficient mice with α7 nicotinic acetylcholine receptor agonists.
Article in Biochemical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Pro-Inflammatory Protein PSCA Is Upregulated in Neurological Diseases and Targets β2-Subunit-Containing nAChRs.Biomolecules · 2025Article
- Neuroprotection: Targeting Multiple Pathways by Naturally Occurring Phytochemicals.Biomedicines · 2020Review
- Development of disease-modifying drugs for frontotemporal dementia spectrum disorders.Nature reviews. Neurology · 2020Review
- Use of Cholinesterase Inhibitors in Non-Alzheimer's Dementias.Drugs & aging · 2019Review
- Reduction of microglial progranulin does not exacerbate pathology or behavioral deficits in neuronal progranulin-insufficient mice.Neurobiology of disease · 2019Article
- Astrocytes and Microglia as Potential Contributors to the Pathogenesis ofFrontiers in neuroscience · 2019Review
- Cerebrospinal fluid soluble TREM2 levels in frontotemporal dementia differ by genetic and pathological subgroup.Alzheimer's research & therapy · 2018Article
- Early microgliosis precedes neuronal loss and behavioural impairment in mice with a frontotemporal dementia-causing CHMP2B mutation.Human molecular genetics · 2017Article
- Progranulin as a candidate biomarker for therapeutic trial in patients with ALS and FTLD.Journal of neural transmission (Vienna, Austria : 1996) · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the progranulin gene cause frontotemporal dementia (FTD), a debilitating neurodegenerative disease that involves atrophy of the frontal and temporal lobes and affects personality, behavior, and language. Progranulin-deficient mouse models of FTD exhibit deficits in compulsive and social behaviors reminiscent of patients with FTD, and develop excessive microgliosis and increased release of inflammatory cytokines. Activation of nicotinic acetylcholine receptors (nAChRs) by nicotine or specific α7 nAChR agonists reduces neuroinflammation. Here, we investigated whether activation of nAChRs by nicotine or α7 agonists improved the excessive inflammatory and behavioral phenotypes of a progranulin-deficient FTD mouse model. We found that treatment with selective α7 agonists, PHA-568487 or ABT-107, strongly suppressed the activation of NF-κB in progranulin-deficient cells. Treatment with ABT-107 also reduced microgliosis, decreased TNFα levels, and reduced compulsive behavior in progranulin-deficient mice. Collectively, these data suggest that targeting activation of the α7 nAChR pathway may be beneficial in decreasing neuroinflammation and reversing some of the behavioral deficits observed in progranulin-deficient FTD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.