ArticleJournal of Alzheimer's disease : JAD2014
Late-onset Alzheimer's disease, heating up and foxed by several proteins: pathomolecular effects of the aging process.
Article in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 29 citations in OpenAlex.
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- Neurostimulation devices to treat Alzheimer's disease.Exploration of neuroscience · 2025Article
- Tubastrine, an antioxidant molecule from Tubastraea tagusensis sun coral, in the reversion of oxidative stress and neuron's death induced by Aβ42.Journal of cellular and molecular medicine · 2024Article
- HDAC6 modulates the cognitive behavioral function and hippocampal tissue pathological changes of APP/PS1 transgenic mice through HSP90-HSF1 pathway.Experimental brain research · 2024Article
- Autophagy-lysosomal pathway impairment and cathepsin dysregulation in Alzheimer's disease.Frontiers in molecular biosciences · 2024Review
- Electromagnetic Field Stimulation Therapy for Alzheimer's Disease.Neurology (Chicago, Ill.) · 2024Article
- Multidimensional insights into the repeated electromagnetic field stimulation and biosystems interaction in aging and age-related diseases.Journal of biomedical science · 2022Review
- Based on molecular structures: Amyloid-β generation, clearance, toxicity and therapeutic strategies.Frontiers in molecular neuroscience · 2022Review
- Repeated electromagnetic field stimulation lowers amyloid-β peptide levels in primary human mixed brain tissue cultures.Scientific reports · 2021Article
- Microvascular Alterations in Alzheimer's Disease.Frontiers in cellular neuroscience · 2020Review
- Alfalfa-derived HSP70 administered intranasally improves insulin sensitivity in mice.Cell stress & chaperones · 2018Article
- Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders.Neurochemical research · 2017Review
- Clearance systems in the brain-implications for Alzheimer disease.Nature reviews. Neurology · 2015Review
- Intravenous immunoglobulin (IVIG) treatment exerts antioxidant and neuropreservatory effects in preclinical models of Alzheimer's disease.Journal of clinical immunology · 2014Article
- Cdk5 activity in the brain - multiple paths of regulation.Journal of cell science · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Late-onset Alzheimer's disease (LOAD) is the most common neurodegenerative disorder in older adults, affecting over 50% of those over age 85. Aging is the most important risk factor for the development of LOAD. Aging is associated with the decrease in the ability of cells to cope with cellular stress, especially protein aggregation. Here we describe how the process of aging affects pathways that control the processing and degradation of abnormal proteins including amyloid-β (Aβ). Genetic association studies in LOAD have successfully identified a large number of genetic variants involved in the development of the disease. However, there is a gap in understanding the interconnections between these pathomolecular events that prevent us from discovering therapeutic targets. We propose novel, pertinent links to elucidate how the biology of aging affects the sequence of events in the development of LOAD. Furthermore we analyze and synthesize the molecular-pathologic-clinical correlations of the aging process, involving the HSF1 and FOXO family pathways, Aβ metabolic pathway, and the different clinical stages of LOAD. Our new model postulates that the aging process would precede Aβ accumulation, and attenuation of HSF1 is an "upstream" event in the cascade that results in excess Aβ and synaptic dysfunction, which may lead to cognitive impairment and/or trigger "downstream" neurodegeneration and synaptic loss. Specific host factors, such as the activity of FOXO family pathways, would mediate the response to Aβ toxicity and the pace of progression toward the clinical manifestations of AD.
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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.