ArticleMolecular brain2018
Lentivirus-mediated expression of human secreted amyloid precursor protein-alpha prevents development of memory and plasticity deficits in a mouse model of Alzheimer's disease.
Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- Virus-mediated gene transfer of soluble amyloid precursor protein-alpha via systemic injection in a mouse model of Alzheimer's disease.Gene therapy · 2026Article
- APOE-ε4 genotype and western diet synergistically aggravate synaptic dysfunction in Alzheimer's disease via D-serine disruption.Alzheimer's research & therapy · 2026Article
- Neurotrophic factor alpha 1 gene therapy in Alzheimer's disease: scope and advancements.Frontiers in molecular neuroscience · 2025Review
- Dysregulated expression of miR-140 and miR-122 compromised microglial chemotaxis and led to reduced restriction of AD pathology.Journal of neuroinflammation · 2024Article
- Article
- Therapeutic effects of a novel synthetic α-secretase.Frontiers in aging neuroscience · 2024Article
- Mechanisms and Functions of Activity-Regulated Cytoskeleton-Associated Protein in Synaptic Plasticity.Molecular neurobiology · 2023Review
- The Q/R editing site of AMPA receptor GluA2 subunit acts as an epigenetic switch regulating dendritic spines, neurodegeneration and cognitive deficits in Alzheimer's disease.Molecular neurodegeneration · 2023Article
- The Amyloid Precursor Protein Regulates Synaptic Transmission at Medial Perforant Path Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Secreted Amyloid Precursor Protein Alpha (sAPPα) Regulates the Cellular Proteome and Secretome of Mouse Primary Astrocytes.International journal of molecular sciences · 2023Article
- Improved NMDA Receptor Activation by the Secreted Amyloid-Protein Precursor-α in Healthy Aging: A Role for D-Serine?International journal of molecular sciences · 2022Article
- APPsα Rescues Tau-Induced Synaptic Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Partial Endothelial Nitric Oxide Synthase Deficiency Exacerbates Cognitive Deficit and Amyloid Pathology in the APPswe/PS1ΔE9 Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Effect of soluble amyloid precursor protein-alpha on adult hippocampal neurogenesis in a mouse model of Alzheimer's disease.Molecular brain · 2022Article
- Secreted Amyloid Precursor Protein Alpha, a Neuroprotective Protein in the Brain Has Widespread Effects on the Transcriptome and Proteome of Human Inducible Pluripotent Stem Cell-Derived Glutamatergic Neurons Related to Memory Mechanisms.Frontiers in neuroscience · 2022Article
- Altered membrane properties but unchanged intrinsic excitability and spontaneous postsynaptic currents in an aged APPFrontiers in cellular neuroscience · 2022Article
- Choroid plexus APP regulates adult brain proliferation and animal behavior.Life science alliance · 2021Article
- APPsα rescues impaired CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Amyloid-Beta Mediates Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Secreted Amyloid Precursor Protein-Alpha Enhances LTP Through the Synthesis and Trafficking of CaFrontiers in molecular neuroscience · 2021Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease driven in large part by accumulated deposits in the brain of the amyloid precursor protein (APP) cleavage product amyloid-β peptide (Aβ). However, AD is also characterised by reductions in secreted amyloid precursor protein-alpha (sAPPα), an alternative cleavage product of APP. In contrast to the neurotoxicity of accumulated Αβ, sAPPα has many neuroprotective and neurotrophic properties. Increasing sAPPα levels has the potential to serve as a therapeutic treatment that mitigates the effects of Aβ and rescue cognitive function. Here we tested the hypothesis that lentivirus-mediated expression of a human sAPPα construct in a mouse model of AD (APPswe/PS1dE9), begun before the onset of plaque pathology, could prevent later behavioural and electrophysiological deficits. Male mice were given bilateral intra-hippocampal injections at 4 months of age and tested 8-10 months later. Transgenic mice expressing sAPPα performed significantly better than untreated littermates in all aspects of the spatial water maze task. Expression of sAPPα also resulted in partial rescue of long-term potentiation (LTP), tested in vitro. These improvements occurred in the absence of changes in amyloid pathology. Supporting these findings on LTP, lentiviral-mediated expression of sAPPα for 3 months from 10 months of age, or acute sAPPα treatment in hippocampal slices from 18 to 20 months old transgenic mice, completely reversed the deficits in LTP. Together these findings suggest that sAPPα has wide potential to act as either a preventative or restorative therapeutic treatment in AD by mitigating the effects of Aβ toxicity and enhancing cognitive reserve.
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