ArticleInternational journal of Alzheimer's disease2012
Protein tau: prime cause of synaptic and neuronal degeneration in Alzheimer's disease.
Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 63 citations in OpenAlex.
- Alzheimer's disease: where do we stand now and what are the strategic interventions?Frontiers in cellular neuroscience · 2025Review
- MicroRNA-219 in the central nervous system: a potential theranostic approach.Research in pharmaceutical sciences · 2024Review
- Early Diagnosis of Neurodegenerative Diseases: What Has Been Undertaken to Promote the Transition from PET to Fluorescence Tracers.Molecules (Basel, Switzerland) · 2024Review
- Blood-brain barrier dysfunction and Alzheimer's disease: associations, pathogenic mechanisms, and therapeutic potential.Frontiers in aging neuroscience · 2023Review
- Mechanistic Insights into Selective Autophagy Subtypes in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2021Review
- Alzheimer's Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia.International journal of molecular sciences · 2021Review
- Pharmacological Modulators of Tau Aggregation and Spreading.Brain sciences · 2020Review
- MicroRNA dynamics during hibernation of the Australian central bearded dragon (Pogona vitticeps).Scientific reports · 2020Article
- Impact of Tau on Neurovascular Pathology in Alzheimer's Disease.Frontiers in neurology · 2020Review
- Article
- Cholinesterase targeting by polyphenols: A therapeutic approach for the treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2018Review
- Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration.Frontiers in neuroscience · 2018Review
- Tau Phosphorylation in Female Neurodegeneration: Role of Estrogens, Progesterone, and Prolactin.Frontiers in endocrinology · 2018Review
- The role of exosomes in the pathogenesis of Alzheimer' disease.Translational neurodegeneration · 2017Review
- Neuroprotective effect of peptides extracted from walnut (Juglans Sigilata Dode) proteins on Aβ25-35-induced memory impairment in mice.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer's disease.Neural regeneration research · 2015Article
- Role of Liver X Receptor in AD Pathophysiology.PloS one · 2015Article
- Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair.DNA repair · 2014Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microtubule-associated protein Tau (MAPT) is a major component of the pathogenesis of a wide variety of brain-damaging disorders, known as tauopathies. These include Alzheimer's disease (AD), denoted as secondary tauopathy because of the obligatory combination with amyloid pathology. In all tauopathies, protein Tau becomes aberrantly phosphorylated, adopts abnormal conformations, and aggregates into fibrils that eventually accumulate as threads in neuropil and as tangles in soma. The argyrophilic neurofibrillary threads and tangles, together denoted as NFT, provide the postmortem pathological diagnosis for all tauopathies. In AD, neurofibrillary threads and tangles (NFTs) are codiagnostic with amyloid depositions but their separated and combined contributions to clinical symptoms remain elusive. Importantly, NFTs are now considered a late event and not directly responsible for early synaptic dysfunctions. Conversely, the biochemical and pathological timeline is not exactly known in human tauopathy, but experimental models point to smaller Tau-aggregates, termed oligomers or multimers, as synaptotoxic in early stages. The challenge is to molecularly define these Tau-isoforms that cause early cognitive and synaptic impairments. Here, we discuss relevant studies and data obtained in our mono- and bigenic validated preclinical models, with the perspective of Tau as a therapeutic target.
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.