ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Minocycline reduces microglial activation and improves behavioral deficits in a transgenic model of cerebral microvascular amyloid.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.
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Who cites it
120 citing papers in PubMed, 1 synthesis or guideline pooled it, 195 citations in OpenAlex.
- Drug repositioning for Alzheimer's disease.Nature reviews. Drug discovery · 2012Pooled it
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- MiR‑204‑5p modulates glial morphology and apomorphine‑induced rotational asymmetry without dopaminergic neuroprotection in a preclinical mouse model of Parkinson's disease.Metabolic brain disease · 2026Article
- Minocycline-Mediated Inhibition of Microglial Activation in Neuroinflammation-Related Neuropsychiatric Disorders: Preclinical Promise and Clinical Limitations.International journal of molecular sciences · 2026Review
- Auranofin reimagined: an emerging therapeutic candidate for neurodegenerative diseases through molecular mechanistic insights.Inflammopharmacology · 2026Review
- Glial-Dopamine crosstalk: Astrocytic and microglial gatekeepers of neuroinflammation, plasticity, and motivation.AIMS neuroscience · 2026Review
- Drug repurposing for Alzheimer's disease using a graph-of-thoughts based large language model to infer drug-disease relationships in a comprehensive knowledge graph.BioData mining · 2025Article
- Doxycycline: An essential tool for Alzheimer's disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Stress-Induced Sleep Dysregulation: The Roles of Astrocytes and Microglia in Neurodegenerative and Psychiatric Disorders.Biomedicines · 2025Review
- Cerebral proteome adaptations to amyloid angiopathy are prevented by carbonic anhydrase inhibitors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Reduction of orexin-expressing neurons and a unique sleep phenotype in the Tg-SwDI mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Loss of TREM2 diminishes CAA despite an overall increase of amyloid load in Tg-SwDI mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Skin-brain axis in Alzheimer's disease - Pathologic, diagnostic, and therapeutic implications: A Hypothetical Review.Aging and disease · 2024Review
- Neurodevelopmental and Neuropsychiatric Disorders.Advances in neurobiology · 2024Review
- Critical thinking of Alzheimer's transgenic mouse model: current research and future perspective.Science China. Life sciences · 2023Review
- Article
- Pathogenic Microglia Orchestrate Neurotoxic Properties of Eomes-Expressing Helper T Cells.Cells · 2023Article
- Enhanced Targeted Delivery of Minocycline via Transferrin Conjugated Albumin Nanoparticle Improves Neuroprotection in a Blast Traumatic Brain Injury Model.Brain sciences · 2023Article
- Inhibiting microglia exacerbates the early effects of cuprizone in males in a rat model of multiple sclerosis, with no effect in females.Frontiers in neurology · 2023Article
60 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cerebral microvascular amyloid beta protein (Abeta) deposition and associated neuroinflammation is increasingly recognized as an important component leading to cognitive impairment in Alzheimer's disease and related cerebral amyloid angiopathy disorders. Transgenic mice expressing the vasculotropic Dutch/Iowa (E693Q/D694N) mutant human Abeta precursor protein in brain (Tg-SwDI) accumulate abundant cerebral microvascular fibrillar amyloid deposits and exhibit robust neuroinflammation. In the present study, we investigated the effect of the anti-inflammatory drug minocycline on Abeta accumulation, neuroinflammation, and behavioral deficits in Tg-SwDI mice. Twelve-month-old mice were treated with saline or minocycline by intraperitoneal injection every other day for a total of 4 weeks. During the final week of treatment, the mice were tested for impaired learning and memory. Brains were then harvested for biochemical and immunohistochemical analysis. Minocycline treatment did not alter the cerebral deposition of Abeta or the restriction of fibrillar amyloid to the cerebral microvasculature. Similarly, minocycline-treated Tg-SwDI mice exhibited no change in the levels of total Abeta, the ratios of Abeta40 and Abeta42, or the amounts of soluble, insoluble, or oligomeric Abeta compared with the saline-treated control Tg-SwDI mice. In contrast, the numbers of activated microglia and levels of interleukin-6 were significantly reduced in minocycline-treated Tg-SwDI mice compared with saline-treated Tg-SwDI mice. In addition, there was a significant improvement in behavioral performance of the minocycline-treated Tg-SwDI mice. These finding suggest that anti-inflammatory treatment targeted for cerebral microvascular amyloid-induced microglial activation can improve cognitive deficits without altering the accumulation and distribution of Abeta.
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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.