ReviewFrontiers in molecular neuroscience2016
The Role of the Carboxyl-Terminal Sequence of Tau and MAP2 in the Pathogenesis of Dementia.
Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular and subregion mechanisms of episodic memory phenotypes in temporal lobe epilepsy.Brain communications · 2022Article
- Medial septum tau accumulation induces spatial memory deficit via disrupting medial septum-hippocampus cholinergic pathway.Clinical and translational medicine · 2021Article
- Tubulin and Tubulin Posttranslational Modifications in Alzheimer's Disease and Vascular Dementia.Frontiers in aging neuroscience · 2021Review
- Phosphatidylinositol-3-OH kinase signalling is spatially organized at endosomal compartments by microtubule-associated protein 4.Nature cell biology · 2020Article
- Ensemble disease gene prediction by clinical sample-based networks.BMC bioinformatics · 2020Article
- Distribution of endogenous normal tau in the mouse brain.The Journal of comparative neurology · 2019Article
- Imbalanced Expression of Tau and Tubulin Induces Neuronal Dysfunction inFrontiers in neuroscience · 2018Article
- Bis(9)-(-)-Meptazinol, a novel dual-binding AChE inhibitor, rescues cognitive deficits and pathological changes in APP/PS1 transgenic mice.Translational neurodegeneration · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dementia includes several diseases characterized by acquired and irreversible brain dysfunctions that interfere with daily life. According to the etiology, dementia can be induced by poisoning or metabolic disorders, and other cases of dementia have a clear pathogenesis. However, half of neurodegenerative diseases have an unclear pathogenesis and etiology. Alzheimer's disease (AD), Lewy body dementia and frontal-temporal dementia are the three most common types of dementia. These neurodegenerative diseases are characterized by the appearance of the following specific protein inclusions: amyloid beta and tau in AD; α-synuclein in Lewy body dementia; and tau, TDP-43, or FUS in frontal-temporal dementia. Thus far, studies on the pathogenesis of dementia mainly focus aberrant inclusions formed by the aforementioned proteins. As a historically heavily studied protein tau is likely to be associated with the pathogenesis of several neurodegenerative diseases that cause dementia. The role of tau in neurodegeneration has been unknown for many years. However, both pathological and genetic analyses have helped tau become gradually recognized as an important factor in the pathogenesis of tauopathy. Currently, especially in the field of AD, tau is attracting more attention and is being considered a potential target for drug development. In this review article, previously discovered biochemical and pathological features of tau are highlighted, and current opinions regarding the neurotoxicity of tau are summarized. Additionally, we introduce key amino acid sequences responsible for tau neurotoxicity from our studies using transgenic
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