Feed Preview

Fast Growing

Tau Toxicity in the Synapses

nobeastsofierce, Shutterstock

Tau toxicity has been implicated in the emergence of synaptic dysfunction in Alzheimer's disease. Here is the latest research on Tau Toxicity in the Synapses.

Top 20 most recent papers

25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner

bioRxivJanuary 15, 2020

Man Ying WongWenjie Luo

Interneuron Accumulation of Phosphorylated tau Impairs Adult Hippocampal Neurogenesis by Suppressing GABAergic Transmission

Cell Stem CellJanuary 25, 2020

Jie ZhengJian-Zhi Wang

Imaging Biomarkers of Alzheimer's Disease in Multiple Sclerosis

Annals of NeurologyJanuary 24, 2020

Burcu ZeydanKejal Kantarci

Loss of function of the mitochondrial peptidase PITRM1 induces proteotoxic stress and Alzheimer's disease-like pathology in human cerebral organoids

bioRxivJanuary 27, 2020

Michela DeleidiCarlo Viscomi

Release of a disordered domain enhances HspB1 chaperone activity toward tau

Proceedings of the National Academy of Sciences of the United States of AmericaJanuary 25, 2020

Hannah E R BaughmanRachel E Klevit

GPCR-mediated clearance of tau in post-synaptic compartments attenuates tau pathology in vivo

bioRxivJanuary 23, 2020

Natura MyekuKaren E Duff

Rho-kinase ROCK inhibitors reduce oligomeric tau protein

Neurobiology of AgingJanuary 27, 2020

Tadanori HamanoYasunari Nakamoto

Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men

NeurologyJanuary 10, 2020

Christian BenedictJonathan Cedernaes

130

Effect Modifiers of TDP-43 Associated Hippocampal Atrophy Rates in Patients with Alzheimer's Disease Neuropathological Changes

Journal of Alzheimer's Disease : JADJanuary 14, 2020

Marina BuciucKeith A Josephs

Regional and temporal miRNAs expression profile in a transgenic mouse model of tauopathy: implication for its pathogenesis

Molecular PsychiatryJanuary 29, 2020

Elisabetta LaurettiDomenico Praticò

Pine Bark Polyphenolic Extract Attenuates Amyloid-β and Tau Misfolding in a Model System of Alzheimer's Disease Neuropathology

Journal of Alzheimer's Disease : JADJanuary 21, 2020

Kenjiro OnoGiulio Maria Pasinetti

ACE2 activation protects against cognitive decline and reduces amyloid pathology in the Tg2576 mouse model of Alzheimer's disease

Acta NeuropathologicaJanuary 27, 2020

Charles E EvansPatrick G Kehoe

Interactive Effects of Racial Identity and Repetitive Head Impacts on Cognitive Function, Structural MRI-Derived Volumetric Measures, and Cerebrospinal Fluid Tau and Aβ

Frontiers in Human NeuroscienceJanuary 11, 2020

Michael L AloscoRobert A Stern

β-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3β/tau cascade

Science Translational MedicineJanuary 17, 2020

Fang ZhangQin Wang

Computer-Aided Drug Design of β-Secretase, γ-Secretase and Anti-Tau Inhibitors for the Discovery of Novel Alzheimer's Therapeutics

International Journal of Molecular SciencesJanuary 25, 2020

Varnavas D MouchlisAntreas Afantitis

Picalm reduction exacerbates tau pathology in a murine tauopathy model

Acta NeuropathologicaJanuary 12, 2020

Kunie AndoJean-Pierre Brion

A pharmacological chaperone improves memory by reducing Aβ and tau neuropathology in a mouse model with plaques and tangles

Molecular NeurodegenerationJanuary 23, 2020

Jian-Guo LiDomenico Praticò

Late-life obesity is a protective factor for prodromal Alzheimer's disease: a longitudinal study

AgingJanuary 28, 2020

Zhen SunAlzheimer’s Disease Neuroimaging Initiative

Direct Interaction between the β-Amyloid Core and Tau Facilitates Cross-Seeding: A Novel Target for Therapeutic Intervention

BiochemistryJanuary 17, 2020

Timir Tripathi, Heena Khan

Resveratrol Protects Optic Nerve Head Astrocytes from Oxidative Stress-Induced Cell Death by Preventing Caspase-3 Activation, Tau Dephosphorylation at Ser422 and Formation of Misfolded Protein Aggregates

Cellular and Molecular NeurobiologyJanuary 11, 2020

John C MeansPeter Koulen

See more papers from this feed

Related Feeds

ALS

Amyotrophic Lateral Sclerosis (ALS), also known as motor neuron disease, is associated with the death of neurons that control voluntary muscles. Discover the latest research on ALS here.

ALS & FTD: TDP-43

ALS shares with a considerable proportion of FTD cases the same neuropathological substrate, namely, inclusions of abnormally phosphorylated protein tdp-43 (ptdp-43). Here are the latest discoveries pertaining to ptdp-43 and these diseases.

ALS - Pathogenic Mechanisms

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. Here is the latest research investigating pathogenic mechanisms that underlie this genetically heterogeneous disorder.

ALS - Phenotypes

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. Here is the latest research investigating phenotypes associated with this genetically heterogeneous disorder.

ALS: Genetics

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. ALS is a genetically heterogeneous disorder with several causative genes. Here are the latest discoveries pertaining to the genetics of this disease.

ALS: Prions

Prions are misfolded proteins which characterize several fatal neurodegenerative diseases. Prion-like mechanisms are associated with the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Here are the latest discoveries pertaining to this disease.

ALS: Stress Granules

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by cytoplasmic protein aggregates within motor neurons. TDP-43 is an ALS-linked protein that is known to regulate splicing and storage of specific mRNAs into stress granules, which have been implicated in formation of ALS protein aggregates. Here is the latest research.

ALS: Therapies

Amyotrophic Lateral Sclerosis (ALS), also known as motor neuron disease, is associated with the death of neurons that control voluntary muscles. Discover the latest research on ALS therapies here.

ALS: Transposon de-silencing

Transposon silencing is a form of transcriptional gene silencing. These gene silencing mechanisms are impaired in Amyotrophic lateral sclerosis (ALS). Here are the latest discoveries pertaining to transposon silencing and this disease.

Age-related Dementia

Age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature. Evidence is reviewed that the neuropathology of the dementia is caused by the breakdown of small cerebral vessels (silent microbleeds), that the microbleeds result from pulse-induced damage to the cerebral vessels, and that pulse becomes increasingly destructive with age, because of the age-related stiffening of the aorta and great arteries, which causes an increase in the intensity of the pressure pulse. Discover the latest research on age-related dementia here.

Contact Help Terms Privacy Cookies