ArticleNeurochemical research2019
Regulation of Neurotransmitter Release by Amyloid Precursor Protein Through Synapsin Phosphorylation.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Loss of intracellular ATP affects axoplasmic viscosity and pathological protein aggregation in mammalian neurons.Science advances · 2025Article
- The reciprocal relationship between amyloid precursor protein and mitochondrial function.Journal of neurochemistry · 2024Review
- Article
- Investigation of the mechanism of tanshinone IIA to improve cognitive function via synaptic plasticity in epileptic rats.Pharmaceutical biology · 2023Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- Disentangling the Amyloid Pathways: A Mechanistic Approach to Etiology.Frontiers in neuroscience · 2020Article
- Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice.Journal of neuroinflammation · 2019Article
- Perturbation of synapsins homeostasis through HIV-1 Tat-mediated suppression of BAG3 in primary neuronal cells.Cell death & disease · 2019Article
- Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases.International journal of molecular sciences · 2018Review
- Synaptic dysfunction in Alzheimer's disease: the effects of amyloid beta on synaptic vesicle dynamics as a novel target for therapeutic intervention.Neural regeneration research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Abnormal processing of amyloid precursor protein (APP) and aggregation of the Aβ peptide are known to play a key role in the pathogenesis of Alzheimer disease, but the function of endogenous APP under normal physiological conditions remains poorly understood. In this study, we investigated presynaptic changes in APP knockout (KO) mice. We demonstrate that both sucrose-induced neurotransmission and synaptic depletion in response to high frequency stimulation are significantly enhanced in APP KO compared to wild type littermates. In addition, the level of phosphorylated forms of synapsins, but not total synapsins, is elevated in the KO mice. Furthermore, we show that the inhibition of L-type calcium channels normalizes phosphorylated synapsins and slows down the high frequency induced synaptic depletion in APP KO mice. These results suggest a new mechanism by which APP regulates synaptic vesicle dynamics through synapsin-dependent phosphorylation.
Indexed as
Identifiers
What OpenQuestion holds
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.