ReviewCNS drugs2016
Aβ-Degrading Proteases: Therapeutic Potential in Alzheimer Disease.
Review in CNS drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Structural and vascular alterations of deep cervical lymph nodes in amyloid PET-positive Alzheimer's disease patients.Cerebral circulation - cognition and behavior · 2026Article
- Volatile oil ofFrontiers in pharmacology · 2025Review
- Coupling of Alzheimer's Disease Genetic Risk Factors with Viral Susceptibility and Inflammation.Aging and disease · 2024Review
- Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.Bioengineering (Basel, Switzerland) · 2024Review
- Suppression of Fli-1 protects against pericyte loss and cognitive deficits in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Article
- Racemization in Post-Translational Modifications Relevance to Protein Aging, Aggregation and Neurodegeneration: Tip of the Iceberg.Symmetry · 2021Article
- Quantitative, High-Throughput Assays for Proteolytic Degradation of Amylin.Methods and protocols · 2020Article
- Shenqi Xingnao Granules ameliorates cognitive impairments and Alzheimer's disease-like pathologies in APP/PS1 mouse model.Chinese herbal medicines · 2020Article
- Molecular Mechanism of Autophagy: Its Role in the Therapy of Alzheimer's Disease.Current neuropharmacology · 2020Review
- Kai-Xin-San, a Chinese Herbal Decoction, Accelerates the Degradation ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism.Molecular neurodegeneration · 2018Article
- Transcriptional Effects of ApoE4: Relevance to Alzheimer's Disease.Molecular neurobiology · 2018Review
- Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer's Disease Model Rats by Maintaining Synaptic Plasticity.CNS & neurological disorders drug targets · 2018Article
- Noradrenergic Dysfunction in Alzheimer's and Parkinson's Diseases-An Overview of Imaging Studies.Frontiers in aging neuroscience · 2018Review
- Extra-virgin olive oil ameliorates cognition and neuropathology of the 3xTg mice: role of autophagy.Annals of clinical and translational neurology · 2017Article
- Haplodeficiency of Cathepsin D does not affect cerebral amyloidosis and autophagy in APP/PS1 transgenic mice.Journal of neurochemistry · 2017Article
- Neuroprotective mechanism ofNeural regeneration research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The amyloid β-protein (Aβ) plays an indispensable role in the pathogenesis of Alzheimer disease (AD). Aβ is subject to proteolytic degradation by a diverse array of peptidases and proteinases, known collectively as Aβ-degrading proteases (AβDPs). A growing number of AβDPs have been identified that impact Aβ powerfully and in a surprising variety of ways. As such, AβDPs hold considerable therapeutic potential for the treatment and/or prevention of AD. Here, we critically review the relative merits of therapeutic strategies targeting AβDPs compared with current Aβ-lowering strategies focused on immunotherapies and pharmacological modulation of Aβ-producing enzymes. Several innovative advances have increased considerably the feasibility of delivering AβDPs to the brain or enhancing their activity in a non-invasive manner. We argue that therapies targeting AβDPs offer numerous potential advantages that should be explored through continued research into this promising field.
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.