ArticleThe Journal of experimental medicine2018
Combination anti-Aβ treatment maximizes cognitive recovery and rebalances mTOR signaling in APP mice.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer's disease model.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Poly(ADP-ribose) Polymerase 1 Deficiency Attenuates Amyloid Pathology, Neurodegeneration, and Cognitive Decline in a Familial Alzheimer's Disease Model.bioRxiv : the preprint server for biology · 2025Article
- Mouse models of Anti-Aβ immunotherapies.Molecular neurodegeneration · 2025Review
- Chemogenetic Tools and their Use in Studies of Neuropsychiatric Disorders.Physiological research · 2024Review
- Altered dynamics of glymphatic flow in a mature-onset Tet-off APP mouse model of amyloidosis.Alzheimer's research & therapy · 2023Article
- A PDK-1 allosteric agonist neutralizes insulin signaling derangements and beta-amyloid toxicity in neuronal cells and in vitro.PloS one · 2022Article
- Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration.Molecular neurodegeneration · 2021Review
- Characterization of the selective in vitro and in vivo binding properties of crenezumab to oligomeric Aβ.Alzheimer's research & therapy · 2019Article
- Rapamycin and Alzheimer's disease: Time for a clinical trial?Science translational medicine · 2019Review
- Gene therapy for neurological disorders: progress and prospects.Nature reviews. Drug discovery · 2018Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Drug development for Alzheimer's disease has endeavored to lower amyloid β (Aβ) by either blocking production or promoting clearance. The benefit of combining these approaches has been examined in mouse models and shown to improve pathological measures of disease over single treatment; however, the impact on cellular and cognitive functions affected by Aβ has not been tested. We used a controllable APP transgenic mouse model to test whether combining genetic suppression of Aβ production with passive anti-Aβ immunization improved functional outcomes over either treatment alone. Compared with behavior before treatment, arresting further Aβ production (but not passive immunization) was sufficient to stop further decline in spatial learning, working memory, and associative memory, whereas combination treatment reversed each of these impairments. Cognitive improvement coincided with resolution of neuritic dystrophy, restoration of synaptic density surrounding deposits, and reduction of hyperactive mammalian target of rapamycin signaling. Computational modeling corroborated by in vivo microdialysis pointed to the reduction of soluble/exchangeable Aβ as the primary driver of cognitive recovery.
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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.