ReviewHandbook of clinical neurology2018
Prion-like mechanisms in Alzheimer disease.
Review in Handbook of clinical neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association of Odor Identification Ability With Amyloid-β and Tau Burden: A Systematic Review and Meta-Analysis.Frontiers in neuroscience · 2020Pooled it
- Phase 1 Studies of the Anti-Tau Monoclonal Antibody JNJ-63733657 in Healthy Participants and Participants with Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2024Trial
- Prion-like transmission and propagation of human β-amyloid to the bank vole rodent model.Acta neuropathologica · 2026Article
- Tau positron emission tomography analysis methods for the quantification of tau spread in preclinical and early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Olfactory decline tracks central-to-peripheral spread of tau pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Human and Mouse Alzheimer's Seeds Differentially Affect Amyloid Deposition and Microglia-Dependent Plaque Response in Aged Mice.Aging cell · 2025Article
- The Role of Air Pollution and Olfactory Dysfunction in Alzheimer's Disease Pathogenesis.Biomedicines · 2025Review
- Linking dietary patterns to Alzheimer's disease biomarkers with network mathematical modeling could enable new approach methodologies in preventative AD research: a narrative interdisciplinary review.Frontiers in nutrition · 2025Review
- Three-dimensional organotypic mouse brain slices to study Alzheimer's disease pathologies: a review.Frontiers in dementia · 2025Review
- Palmitoylation acts as a checkpoint for MAVS aggregation to promote antiviral innate immune responses.The Journal of clinical investigation · 2024Article
- Rapid and sensitive determination of residual prion infectivity from prion-decontaminated surfaces.mSphere · 2024Article
- Article
- Tau seed amplification assay reveals relationship between seeding and pathological forms of tau in Alzheimer's disease brain.Acta neuropathologica communications · 2023Article
- Human amygdala involvement in Alzheimer's disease revealed by stereological and dia-PASEF analysis.Brain pathology (Zurich, Switzerland) · 2023Article
- Recent Trends in Active and Passive Immunotherapies of Alzheimer's Disease.Antibodies (Basel, Switzerland) · 2023Review
- Review
- Prion Protein Octarepeat Domain Forms Transient β-Sheet Structures upon Residue-Specific Binding to Cu(II) and Zn(II) Ions.Biochemistry · 2023Article
- Progressive Spread of Beta-amyloid Pathology in an Olfactory-driven Amyloid Precursor Protein Mouse Model.Neuroscience · 2023Article
- A multi-scale model explains oscillatory slowing and neuronal hyperactivity in Alzheimer's disease.Journal of the Royal Society, Interface · 2023Article
- Modeling the Competition between Misfolded Aβ Conformers That Produce Distinct Types of Amyloid Pathology in Alzheimer's Disease.Biomolecules · 2022Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Senile plaques and neurofibrillary tangles are the principal histopathologic hallmarks of Alzheimer disease. The essential constituents of these lesions are structurally abnormal variants of normally generated proteins: Aβ protein in plaques and tau protein in tangles. At the molecular level, both proteins in a pathogenic state share key properties with classic prions, i.e., they consist of alternatively folded, β-sheet-rich forms of the proteins that autopropagate by the seeded corruption and self-assembly of like proteins. Other similarities with prions include the ability to manifest as polymorphic and polyfunctional strains, resistance to chemical and enzymatic destruction, and the ability to spread within the brain and from the periphery to the brain. In Alzheimer disease, current evidence indicates that the pathogenic cascade follows from the endogenous, sequential corruption of Aβ and then tau. Therapeutic options include reducing the production or multimerization of the proteins, uncoupling the Aβ-tauopathy connection, or promoting the inactivation or removal of anomalous assemblies from the brain. Although aberrant Aβ appears to be the prime mover of Alzheimer disease pathogenesis, once set in motion by Aβ, the prion-like propagation of tauopathy may proceed independently of Aβ; if so, Aβ might be solely targeted as an early preventive measure, but optimal treatment of Alzheimer disease at later stages of the cascade could require intervention in both pathways.
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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.