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Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function

TLDR
NFTs are not sufficient to cause cognitive decline or neuronal death in this model of tauopathy, and after the suppression of transgenic tau, memory function recovered, and neuron numbers stabilized, but to the authors' surprise, NFTs continued to accumulate.
Abstract
Neurofibrillary tangles (NFTs) are the most common intraneuronal inclusion in the brains of patients with neurodegenerative diseases and have been implicated in mediating neuronal death and cognitive deficits Here, we found that mice expressing a repressible human tau variant developed progressive age-related NFTs, neuronal loss, and behavioral impairments After the suppression of transgenic tau, memory function recovered, and neuron numbers stabilized, but to our surprise, NFTs continued to accumulate Thus, NFTs are not sufficient to cause cognitive decline or neuronal death in this model of tauopathy

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The Blood-Brain Barrier in Health and Chronic Neurodegenerative Disorders

TL;DR: These findings support developments of new therapeutic approaches for chronic neurodegenerative disorders directed at the blood-brain barrier and other nonneuronal cells of the neurovascular unit.
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A specific amyloid-|[beta]| protein assembly in the brain impairs memory

TL;DR: It is found that memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-β assembly, which is proposed to be Aβ*56 (Aβ star 56), which may contribute to cognitive deficits associated with Alzheimer's disease.
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Tau-mediated neurodegeneration in Alzheimer's disease and related disorders.

TL;DR: This Review summarizes the most recent advances in knowledge of the mechanisms of tau-mediated neurodegeneration to forge an integrated concept of those t Tau-linked disease processes that drive the onset and progression of AD and related tauopathies.
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A beta oligomers - a decade of discovery.

TL;DR: Accumulating evidence suggests that soluble forms of Aβ are indeed the proximate effectors of synapse loss and neuronal injury in Alzheimer’s disease.
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Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model

TL;DR: Reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Aβ levels, and protected both transgenic and nontransgenic mice against excitotoxicity.
References
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Journal ArticleDOI

Tight control of gene expression in mammalian cells by tetracycline-responsive promoters.

TL;DR: Control elements of the tetracycline-resistance operon encoded in Tn10 of Escherichia coli have been utilized to establish a highly efficient regulatory system in mammalian cells that is suitable for creation of "on/off" situations for such genes in a reversible way.
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Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17

TL;DR: In this paper, the authors sequenced tau in FTDP-17 families and identified three missense mutations (G272V, P301L and R406W) and three mutations in the 5' splice site of exon in
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Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology

TL;DR: It is suggested that tau in Alzheimer brain is an abnormally phosphorylated protein component of PHF, the two major locations of paired-helical filaments in Alzheimer disease brain.
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A protein factor essential for microtubule assembly

TL;DR: The unique ability of tau to restore the normal features of in vitro microtubules assembly makes it likely that tau is a major regulator of microtubule formation in cells.
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Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease

TL;DR: The severity of dementia was positively related to the number of NFTs in neocortex, but not to the degree of SP deposition, and N FTs accumulate in a consistent pattern reflecting hierarchic vulnerability of individual cytoarchitectural fields.
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