ArticleBrain pathology (Zurich, Switzerland)2010
Higher soluble amyloid beta concentration in frontal cortex of young adults than in normal elderly or Alzheimer's disease.
Article in Brain pathology (Zurich, Switzerland), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Modulation of Alzheimer's Disease Aβ40 Fibril Polymorphism by the Small Heat Shock Protein αB-Crystallin.Journal of the American Chemical Society · 2024Article
- Is later-life depression a risk factor for Alzheimer's disease or a prodromal symptom: a study using post-mortem human brain tissue?Alzheimer's research & therapy · 2023Article
- Proteins Do Not Replicate, They Precipitate: Phase Transition and Loss of Function Toxicity in Amyloid Pathologies.Biology · 2022Review
- Importance of CSF-based Aβ clearance with age in humans increases with declining efficacy of blood-brain barrier/proteolytic pathways.Communications biology · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Mediators of cerebral hypoperfusion and blood-brain barrier leakiness in Alzheimer's disease, vascular dementia and mixed dementia.Brain pathology (Zurich, Switzerland) · 2021Article
- A Novel AβScientific reports · 2020Article
- Reversal ofOxidative medicine and cellular longevity · 2020Article
- Cerebral AβJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Clusterin levels are increased in Alzheimer's disease and influence the regional distribution of Aβ.Brain pathology (Zurich, Switzerland) · 2017Article
- Angiotensin-converting enzyme 2 is reduced in Alzheimer's disease in association with increasing amyloid-β and tau pathology.Alzheimer's research & therapy · 2016Article
- Pathophysiology of Hypoperfusion of the Precuneus in Early Alzheimer's Disease.Brain pathology (Zurich, Switzerland) · 2016Article
- Characterization of Amyloid-β Deposits in Bovine Brains.Journal of Alzheimer's disease : JAD · 2016Article
- Early Age-Related Functional Connectivity Decline in High-Order Cognitive Networks.Frontiers in aging neuroscience · 2016Article
- Intrinsic excitability changes induced by acute treatment of hippocampal CA1 pyramidal neurons with exogenous amyloid β peptide.Hippocampus · 2015Article
- Reduced vascular endothelial growth factor and capillary density in the occipital cortex in dementia with Lewy bodies.Brain pathology (Zurich, Switzerland) · 2014Article
- Evaluating the relationship between amyloid-β and α-synuclein phosphorylated at Ser129 in dementia with Lewy bodies and Parkinson's disease.Alzheimer's research & therapy · 2014Article
- Article
- Prion protein is decreased in Alzheimer's brain and inversely correlates with BACE1 activity, amyloid-β levels and Braak stage.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Little is known about the relationship between soluble amyloid beta (Abeta) and age. We have measured soluble and insoluble Abeta by enzyme-linked immunosorbent assay (ELISA) in post-mortem frontal cortex in normal brains (16-95 years) and AD. Insoluble Abeta increased with age, and was significantly higher in Alzheimer's disease (AD) than age-matched controls. However, levels of soluble Abeta declined with age and were significantly greater in younger adults than older adults with or without AD. In AD, insoluble : soluble Abeta ratio was much higher than in age-matched controls. The high levels of soluble Abeta in young adults included oligomeric species of Abeta(1-42). These observations do not preclude Abeta oligomers as neurotoxic mediators of AD but suggest that if they are, the toxicity may be restricted to certain species (eg, beta-pleated protofibrillar species not detected by our assay) or takes decades to manifest. The dramatically increased insoluble : soluble Abeta in AD points to an altered dynamic equilibrium of Abeta in AD, reflecting both enhanced aggregation and continued overproduction or impaired removal of the soluble peptide in older age, when the concentration of this peptide should be declining.
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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.