ReviewJournal of neural transmission (Vienna, Austria : 1996)2015
Brain hypometabolism triggers PHF-like phosphorylation of tau, a major hallmark of Alzheimer's disease pathology.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology.Frontiers in neurology · 2020Pooled it
- Association between lower body temperature and increased tau pathology in cognitively normal older adults.Neurobiology of disease · 2022Trial
- RNA Granules at the Crossroads of Synaptic Dysfunction and Neurodegeneration.Journal of neurochemistry · 2025Review
- Torpor induces reversible tau hyperphosphorylation and accumulation in mice expressing human tau.Acta neuropathologica communications · 2024Article
- Sleep deprivation soon after recovery from synthetic torpor enhances tau protein dephosphorylation in the rat brain.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Article
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Synthetic torpor triggers a regulated mechanism in the rat brain, favoring the reversibility of Tau protein hyperphosphorylation.Frontiers in physiology · 2023Article
- Contrasting Metabolic Insufficiency in Aging and Dementia.Aging and disease · 2021Review
- Phosphorylated Tau protein in the myenteric plexus of the ileum and colon of normothermic rats and during synthetic torpor.Cell and tissue research · 2021Article
- Reversible Tau Phosphorylation Induced by Synthetic Torpor in the Spinal Cord of the Rat.Frontiers in neuroanatomy · 2021Article
- Aβ1-42 and Tau as Potential Biomarkers for Diagnosis and Prognosis of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020Article
- Waking the sleeping dragon: gene expression profiling reveals adaptive strategies of the hibernating reptile Pogona vitticeps.BMC genomics · 2019Article
- Calcium-Binding Proteins in the Nervous System during Hibernation: Neuroprotective Strategies in Hypometabolic Conditions?International journal of molecular sciences · 2019Review
- Activation of the Brain to Postpone Dementia: A Concept Originating from Postmortem Human Brain Studies.Neuroscience bulletin · 2019Review
- Phosphorylation and Dephosphorylation of Tau Protein During Synthetic Torpor.Frontiers in neuroanatomy · 2019Article
- Article
- Untangling the Tauopathy for Alzheimer's disease and parkinsonism.Journal of biomedical science · 2018Review
- Epigenetic dysregulation of brainstem nuclei in the pathogenesis of Alzheimer's disease: looking in the correct place at the right time?Cellular and molecular life sciences : CMLS · 2017Review
- Neuroprotective Effects Against POCD by Photobiomodulation: Evidence from Assembly/Disassembly of the Cytoskeleton.Journal of experimental neuroscience · 2016Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder of unknown cause characterized by fibrillar accumulation of the Aß-peptide and aggregates of the microtubule-associated protein tau in a hyperphosphorylated form. Already at preclinical stages, AD is characterized by hypometabolic states which are a good predictor of cognitive decline. Here, we summarize recent evidence derived from the study of hibernating animals that brain hypometabolism can trigger PHF-like hyperphosphorylation of tau. We put forward the concept that particular types of neurons respond to a hypometabolic state with an elevated phosphorylation of tau protein which represents a physiological mechanism involved in regulating synaptic gain. If, in contrast to hibernation, the hypometabolic state is not terminated after a definite time but rather persists and progresses, the elevated phosphorylation of tau protein endures and the protective reaction associated with it might turn into a pathological cascade leading to neurodegeneration.
Indexed as
Identifiers
25480630What OpenQuestion holds
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.