ReviewNeural plasticity2012
Consequences of inhibiting amyloid precursor protein processing enzymes on synaptic function and plasticity.
Review in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 66 citations in OpenAlex.
- Truncated mini LRP1 transports cargo from luminal to basolateral side across the blood brain barrier.Fluids and barriers of the CNS · 2024Article
- New Evidence on a Distinction between Aβ40 and Aβ42 Amyloids: Thioflavin T Binding Modes, Clustering Tendency, Degradation Resistance, and Cross-Seeding.International journal of molecular sciences · 2022Article
- Aerobic Exercise Regulates Apoptosis through the PI3K/Akt/GSK-3Neural plasticity · 2022Article
- Structural Studies Providing Insights into Production and Conformational Behavior of Amyloid-β Peptide Associated with Alzheimer's Disease Development.Molecules (Basel, Switzerland) · 2021Review
- Disentangling the Amyloid Pathways: A Mechanistic Approach to Etiology.Frontiers in neuroscience · 2020Article
- Reciprocal modulation between amyloid precursor protein and synaptic membrane cholesterol revealed by live cell imaging.Neurobiology of disease · 2019Article
- TheFrontiers in neuroscience · 2019Article
- Novel Insights into the Physiological Function of the APP (Gene) Family and Its Proteolytic Fragments in Synaptic Plasticity.Frontiers in molecular neuroscience · 2016Review
- Killing Me Softly: Connotations to Unfolded Protein Response and Oxidative Stress in Alzheimer's Disease.Oxidative medicine and cellular longevity · 2016Review
- Functional Characteristics and Molecular Mechanism of a New scFv Antibody Against Aβ42 Oligomers and Immature Protofibrils.Molecular neurobiology · 2015Article
- Loss of Spatial Memory, Learning, and Motor Function During Normal Aging Is Accompanied by Changes in Brain Presenilin 1 and 2 Expression Levels.Molecular neurobiology · 2015Article
- Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease.Acta neuropathologica communications · 2014Review
- Protein prenylation and synaptic plasticity: implications for Alzheimer's disease.Molecular neurobiology · 2014Review
- BACE1 is necessary for experience-dependent homeostatic synaptic plasticity in visual cortex.Neural plasticity · 2014Article
- Effects of (-)Epicatechin on the Pathology of APP/PS1 Transgenic Mice.Frontiers in neurology · 2014Article
- Postsynaptic target specific synaptic dysfunctions in the CA3 area of BACE1 knockout mice.PloS one · 2014Article
- A new treatment for cognitive disorders related to in utero exposure to alcohol.Neural regeneration research · 2013Article
- A tetra(ethylene glycol) derivative of benzothiazole aniline enhances Ras-mediated spinogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Is sleep essential for neural plasticity in humans, and how does it affect motor and cognitive recovery?Neural plasticity · 2013Review
- Postsynaptic dysfunction is associated with spatial and object recognition memory loss in a natural model of Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease, one of whose major pathological hallmarks is the accumulation of amyloid plaques comprised of aggregated β-amyloid (Aβ) peptides. It is now recognized that soluble Aβ oligomers may lead to synaptic dysfunctions early in AD pathology preceding plaque deposition. Aβ is produced by a sequential cleavage of amyloid precursor protein (APP) by the activity of β- and γ-secretases, which have been identified as major candidate therapeutic targets of AD. This paper focuses on how Aβ alters synaptic function and the functional consequences of inhibiting the activity of the two secretases responsible for Aβ generation. Abnormalities in synaptic function resulting from the absence or inhibition of the Aβ-producing enzymes suggest that Aβ itself may have normal physiological functions which are disrupted by abnormal accumulation of Aβ during AD pathology. This interpretation suggests that AD therapeutics targeting the β- and γ-secretases should be developed to restore normal levels of Aβ or combined with measures to circumvent the associated synaptic dysfunction(s) in order to have minimal impact on normal synaptic function.
Indexed as
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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.