ReviewCurrent Alzheimer research2011
A novel perspective on tau in Alzheimer's disease.
Review in Current Alzheimer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Neuronal gene profiling of tau oligomer-bearing cholinergic nucleus basalis neurons during the onset of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Rational Modulation of Liquid-Liquid Phase Separation Offers Novel Ways to Combat Tauopathies.International journal of molecular sciences · 2025Review
- Emerging Links Between Ferroptosis and Neurodegeneration: Implications for Disease Mechanisms and Nutraceutical Interventions.Food science & nutrition · 2025Review
- Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress.Nature neuroscience · 2024Article
- MicroRNAs: pioneering regulators in Alzheimer's disease pathogenesis, diagnosis, and therapy.Translational psychiatry · 2024Review
- Untangling Tau: Molecular Insights into Neuroinflammation, Pathophysiology, and Emerging Immunotherapies.Current issues in molecular biology · 2023Review
- Tau Oligomers Neurotoxicity.Life (Basel, Switzerland) · 2021Review
- Ferroptosis Mechanisms Involved in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Isorhynchophylline alleviates learning and memory impairments induced by aluminum chloride in mice.Chinese medicine · 2018Article
- Docking Studies and Biological Evaluation of a Potential β-Secretase Inhibitor of 3-Hydroxyhericenone F fromFrontiers in pharmacology · 2017Article
- PARK2 enhancement is able to compensate mitophagy alterations found in sporadic Alzheimer's disease.Human molecular genetics · 2016Article
- Oxidative Stress in Alzheimer's Disease: Should We Keep Trying Antioxidant Therapies?Cellular and molecular neurobiology · 2015Review
- Modification of the Drosophila model of in vivo Tau toxicity reveals protective phosphorylation by GSK3β.Biology open · 2014Article
- Zinc and the aging brain.Genes & nutrition · 2014Article
- Article
- The senescence hypothesis of disease progression in Alzheimer disease: an integrated matrix of disease pathways for FAD and SAD.Molecular neurobiology · 2013Review
- Deconstructing mitochondrial dysfunction in Alzheimer disease.Oxidative medicine and cellular longevity · 2013Review
- Early Alzheimer's and Parkinson's disease pathology in urban children: Friend versus Foe responses--it is time to face the evidence.BioMed research international · 2013Review
- A new link to mitochondrial impairment in tauopathies.Molecular neurobiology · 2012Article
- Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's disease.Brain research · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Mainstream thinking is dominated by the notion that the aggregation of specific proteins within neurons, and their subsequent formation into cytoplasmic and extracellular lesions, directly elicits neuronal dysfunction and death. Current dogma, for example, maintains that phosphorylated tau protein, the major component of neurofibrillary tangles, is a central mediator of disease pathogenesis. In this article, we challenge this classic notion by proposing that tau phosphorylation represents a compensatory response mounted by neurons against oxidative stress that serves a protective function. This concept provides a better understanding of the mechanisms underlying disease pathophysiology and also provides a window for therapeutic intervention.
Indexed as
Identifiers
What 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.