ArticleJournal of Alzheimer's parkinsonism & dementia2016
Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer's Disease?
Article in Journal of Alzheimer's parkinsonism & dementia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 50 citations in OpenAlex.
- Japanese participant data from three gantenerumab trials in early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.Molecular neurobiology · 2025Review
- ACognitive neurodynamics · 2024Article
- Inhibition of Soluble Epoxide Hydrolase Ameliorates Cerebral Blood Flow Autoregulation and Cognition in Alzheimer's Disease and Diabetes-Related Dementia Rat Models.bioRxiv : the preprint server for biology · 2024Article
- Anthocyanin-Rich Fraction of Black Rice Bran Extract Protects against Amyloid β-Induced Oxidative Stress, Endoplasmic Reticulum Stress, and Neuronal Apoptosis in SK-N-SH Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The duality of amyloid-β: its role in normal and Alzheimer's disease states.Molecular brain · 2024Review
- Impact of multiple infections on risk of incident dementia according to subjective cognitive decline status: a nationwide population-based cohort study.Frontiers in aging neuroscience · 2024Article
- Image-guided subject-specific modeling of glymphatic transport and amyloid deposition.Computer methods in applied mechanics and engineering · 2023Article
- Role ofbioRxiv : the preprint server for biology · 2023Article
- Review
- Amyloid Fibrils ofInternational journal of molecular sciences · 2023Article
- Longitudinal characterization of cerebral hemodynamics in the TgF344-AD rat model of Alzheimer's disease.GeroScience · 2023Article
- Review
- Enhanced Cerebral Hemodynamics and Cognitive Function Via Knockout of Dual-Specificity Protein Phosphatase 5.Journal of pharmacy and pharmacology research · 2023Article
- Systolic Blood Pressure Is Associated with Increased Brain Amyloid Load in Mild Cognitively Impaired Participants: Alzheimer's Disease Neuroimaging Initiatives Study.Dementia and geriatric cognitive disorders · 2023Article
- Amyloid fibrils degradation: the pathway to recovery or aggravation of the disease?Frontiers in molecular biosciences · 2023Article
- BACE1 Inhibitors for Alzheimer's Disease: The Past, Present and Any Future?Molecules (Basel, Switzerland) · 2022Review
- Multi-Omics-Based Autophagy-Related Untypical Subtypes in Patients with Cerebral Amyloid Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by the pathological hallmarks of extracellular beta-amyloid (Aβ) plaques and intraneuronal tau-containing neurofibrillary tangles in the brain. Intraneuronal accumulation of Aβ also plays a role to accelerate AD progression by promoting neurodegeneration. Additionally, AD is associated with the development of amyloid angiopathy (CAA), in which Aβ builds up on the walls of the cerebral arteries, which augments the development of cerebral vascular disease (CVD). Conversely, CVD promotes Aβ deposition and the development of AD by affecting the balance of Aβ production and clearance. However, it remains to be determined whether the accumulation of Aβ is a cause or consequence of AD. The interaction between AD and CVD is a topic of considerable current interest. Here, we discuss the role of CVD in Aβ accumulation and the development of AD to provide a new point of view that combination therapies that address the accompanying cerebral microvascular disease may potentiate the efficacy of emerging treatment for AD.
Indexed as
Identifiers
28815226PMC5555607W2983597664What 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.