ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2012
Is Alzheimer's disease amyloidosis the result of a repair mechanism gone astray?
Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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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.
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Who cites it
8 citing papers in PubMed, 29 citations in OpenAlex.
- Neuroinflammation and Neurogenesis in Alzheimer's Disease and Potential Therapeutic Approaches.International journal of molecular sciences · 2020Review
- A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease.Nature reviews. Neurology · 2019Review
- Biochemical assessment of precuneus and posterior cingulate gyrus in the context of brain aging and Alzheimer's disease.PloS one · 2014Article
- Neurochemical profile of dementia pugilistica.Journal of neurotrauma · 2013Article
- Bapineuzumab alters aβ composition: implications for the amyloid cascade hypothesis and anti-amyloid immunotherapy.PloS one · 2013Article
- Interactions between amyloid-β and hemoglobin: implications for amyloid plaque formation in Alzheimer's disease.PloS one · 2012Article
- Morphological and pathological evolution of the brain microcirculation in aging and Alzheimer's disease.PloS one · 2012Article
- A Cross-Sectional Analysis of Late-Life Cardiovascular Factors and Their Relation to Clinically Defined Neurodegenerative Diseases.Alzheimer disease and associated disordersArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Here, we synthesize several lines of evidence supporting the hypothesis that at least one function of amyloid-β is to serve as a part of the acute response to brain hemodynamic disturbances intended to seal vascular leakage. Given the resilient and adhesive physicochemical properties of amyloid, an abluminal hemostatic repair system might be highly advantageous, if deployed on a limited and short-term basis, in young individuals. However, in the aged, inevitable cardiovascular dysfunction combined with brain microvascular lesions may yield global chronic hypoperfusion that may lead to continuous amyloid deposition and consequential negative effects on neuronal viability. A large body of experimental evidence supports the hypothesis of an amyloid-β rescue function gone astray. Preventing or inducing the removal of amyloid in Alzheimer's disease (AD) has been simultaneously successful and disappointing. Amyloid deposits clearly play major roles in AD, but they may not represent the preeminent factor in dementia pathogenesis. Successful application of AD preventative approaches may hinge on an accurate and comprehensive view of comorbidities, including cardiovascular disease, diabetes, and head trauma.
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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.