ReviewJournal of Alzheimer's disease : JAD2018
Positive Feedback Loops in Alzheimer's Disease: The Alzheimer's Feedback Hypothesis.
Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 60 citations in OpenAlex.
- A recent review on ginseng's effects on neurodegenerative diseases: active ingredients, mechanisms of action, applications, and delivery strategies.Frontiers in nutrition · 2026Review
- Kinetic Model with Feedback Cycle for Age-Dependent Amyloid Beta Accumulation in Mice.International journal of molecular sciences · 2025Article
- Effects of ion type and concentration on the structure and aggregation of the amyloid peptide AProteins · 2025Article
- Pharmacologically increasing O-GlcNAcylation increases complexity of astrocytes in the dentate gyrus of TgF344-AD rats.Frontiers in aging neuroscience · 2025Article
- Associations Between Skin Microbiome and Metabolome in the Pathogenesis of Atopic Dermatitis Patients With Scalp Involvement.Allergy, asthma & immunology research · 2024Article
- Mind the Gap: Unraveling the Intricate Dance Between Alzheimer's Disease and Related Dementias and Bone Health.Current osteoporosis reports · 2024Review
- Anti-Hypertensives Reduce the Rate of Alzheimer's Disease Progression: A Cohort Study Linked with Genetic and Neuropathological Analyses.The journal of prevention of Alzheimer's disease · 2024Article
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Study insights in the role of PGC-1α in neurological diseases: mechanisms and therapeutic potential.Frontiers in aging neuroscience · 2024Review
- Modulating the RAGE-Induced Inflammatory Response: Peptoids as RAGE Antagonists.Chembiochem : a European journal of chemical biology · 2023Article
- Metformin mitigates amyloid βMetabolic brain disease · 2023Article
- Microglia specific deletion of miR-155 in Alzheimer's disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures.Journal of neuroinflammation · 2023Article
- Thalamocortical bistable switch as a theoretical model of fibromyalgia pathogenesis inferred from a literature survey.Journal of computational neuroscience · 2022Article
- Article
- The amyloid precursor protein: a converging point in Alzheimer's disease.Molecular neurobiology · 2022Review
- Nobiletin prevents amyloid βMetabolic brain disease · 2022Article
- Reactive natural kinds and varieties of dependence.European journal for philosophy of science · 2022Article
- Metabolomic Analysis of Skin Biopsies from Patients with Atopic Dermatitis Reveals Hallmarks of Inflammation, Disrupted Barrier Function and Oxidative Stress.Acta dermato-venereologica · 2021Article
- Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer's Disease, Parkinson's Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis.Chemical reviews · 2021Review
- TRPM2 channel-mediated cell death: An important mechanism linking oxidative stress-inducing pathological factors to associated pathological conditions.Redox biology · 2020Review
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 dominant model for Alzheimer's disease (AD) is the amyloid cascade hypothesis, in which the accumulation of excess amyloid-β (Aβ) leads to inflammation, excess glutamate and intracellular calcium, oxidative stress, tau hyperphosphorylation and tangle formation, neuronal loss, and ultimately dementia. In a cascade, AD proceeds in a unidirectional fashion, with events only affecting downstream processes. Compelling evidence now exists for the presence of positive feedback loops in AD, however, involving oxidative stress, inflammation, glutamate, calcium, and tau. The pathological state of AD is thus a system of positive feedback loops, leading to amplification of the initial perturbation, rather than a linear cascade. Drugs may therefore be effective by targeting numerous points within the loops, rather than concentrating on upstream processes. Anti-inflammatories and anti-oxidants may be especially valuable, since these processes are involved in many loops and hence would affect numerous processes in AD.
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.