ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Small-diffusible aggregates, plaques, tangles, and dynamic equilibria: Untangling Alzheimer's disease.
Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Pathological depositions in human disease: converging mechanisms in atherosclerosis, Alzheimer's disease, and related disorders.Molecular biomedicine · 2026Review
- Lipid Metabolism in Central Nervous System Diseases: Pathological Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Molecular design of MRI probes for targeting amyloid-β species: fromTheranostics · 2026Review
- Small-diffusible aggregates, plaques, tangles, and dynamic equilibria: Untangling Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBeta-amyloid plaques and hyperphosphorylated tau tangles are the neuropathological hallmarks of Alzheimer's disease; however, their relevance in the pathophysiology is not fully understood. It has been suggested that these larger and insoluble aggregates may not be the most toxic forms of beta-amyloid and tau in Alzheimer's disease, and the disease progression may actually be promoted by the small-diffusible aggregates. METHODS AND
resultsWe combine the recent findings from our group and other key research to put forward the hypotheses that the formation of the small-diffusible aggregates of beta-amyloid and tau and their larger insoluble counterparts is not a linear process. DISCUSSION: While the small-diffusible aggregate formation of beta-amyloid and tau is a passive process, regulated by thermodynamic equilibria, the formation of large-insoluble aggregates is an active process, regulated by microglia and neurons, which to an extent is a protective mechanism against the toxicity of the smaller aggregates. HIGHLIGHTS: Plaques and tangles may be made by active processes in Alzheimer's disease. The small-soluble aggregates may be the more toxic species in Alzheimer's disease. Pathology may be caused by the imbalance of production and clearance of aggregates. Plaques and tangle formation may be attempts to restore the homeostatic equilibrium.
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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.