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Scientific Reports (7)
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Showing 1–20 of 20 results

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Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1

Karen Duff
Chris Eckman
Steven Younkin
Research24 Oct 1996
Nature

Volume: 383, P: 710-713
Inhibition of tau neuronal internalization using anti-tau single domain antibodies

Single domain antibodies block tau entry into neurons, a key step in tau propagation in the brain in Alzheimer’s disease. They prevent tau from binding to surface receptors by competition. The most effective, VHH H3-2, has a unique binding mode to tau.

Clément Danis
Elian Dupré
Isabelle Landrieu
ResearchOpen Access02 Apr 2025
Nature Communications

Volume: 16, P: 1-14
Age-related shift in LTD is dependent on neuronal adenosine A_2A receptors interplay with mGluR5 and NMDA receptors

Mariana Temido-Ferreira
Diana G. Ferreira
Luísa V. Lopes
ResearchOpen Access27 Jun 2018
Molecular Psychiatry

Volume: 25, P: 1876-1900
The caffeine-binding adenosine A_2A receptor induces age-like HPA-axis dysfunction by targeting glucocorticoid receptor function

Vânia L. Batalha
Diana G. Ferreira
Luísa V. Lopes
ResearchOpen Access11 Aug 2016
Scientific Reports

Volume: 6, P: 1-15
Reply to: Questioning the cycad theory of Kii ALS–PDC causation

Katerina Menšíková
Raymond Rosales
Petr Kaňovský
Correspondence09 Feb 2024
Nature Reviews Neurology

Volume: 20, P: 195-196
Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats

RNA-binding proteins acting as decoys for pathogenic expanded CUG RNA repeats reverse the toxicity of the mutant transcripts in muscle cells derived from a patient with myotonic dystrophy type 1 and in a mouse model of the disease.

Ludovic Arandel
Magdalena Matloka
Denis Furling
Research10 Feb 2022
Nature Biomedical Engineering

Volume: 6, P: 207-220
Tau accumulation in astrocytes of the dentate gyrus induces neuronal dysfunction and memory deficits in Alzheimer’s disease

Alzheimer’s disease is often considered a disease of neurons. This study reveals that astrocytes are also impaired by the disease and that these cells contribute more to memory deterioration than previously thought.

Kevin Richetin
Pascal Steullet
Nicole Déglon
Research09 Nov 2020
Nature Neuroscience

Volume: 23, P: 1567-1579
NLRP3 inflammasome activation drives tau pathology

The authors show that NLRP3 inflammasome is activated in microglia of patients with fronto-temporal dementia and in a mouse model of tau pathology, and that the loss of NLRP3 inflammasome function decreases tau pathology and improves cognition in mice.

Christina Ising
Carmen Venegas
Michael T. Heneka
Research20 Nov 2019
Nature

Volume: 575, P: 669-673
Upregulation of adenosine A_2A receptor in astrocytes is sufficient to trigger hippocampal multicellular dysfunctions and memory deficits

Agathe Launay
Kevin Carvalho
David Blum
ResearchOpen Access23 Jul 2025
Molecular Psychiatry

Volume: 30, P: 5300-5314
Role of the Tau N-terminal region in microtubule stabilization revealed by newendogenous truncated forms

Maxime Derisbourg
Coline Leghay
Malika Hamdane
ResearchOpen Access14 May 2015
Scientific Reports

Volume: 5, P: 1-10
Effects of the therapeutic correction of U1 snRNP complex on Alzheimer’s disease

Caio Bruno Q. S. Leal
Camila G. M. Zimmer
Rafael M. Bottos
ResearchOpen Access03 Dec 2024
Scientific Reports

Volume: 14, P: 1-17
Endemic parkinsonism: clusters, biology and clinical features

Endemic parkinsonism occurs only in specific locations or populations. Here, Menšíková et al. describe clusters of endemic parkinsonism and highlight that those linked to neurotoxic environmental factors seem to be disappearing, while genetically determined clusters persist.

Katerina Menšíková
John C. Steele
Petr Kaňovský
Reviews08 Sept 2023
Nature Reviews Neurology

Volume: 19, P: 599-616
The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer’s disease

Loan Vaillant-Beuchot
Fanny Eysert
Mounia Chami
ResearchOpen Access28 May 2024
Cell Death & Disease

Volume: 15, P: 1-14
Single cell transcriptome analysis of the THY-Tau22 mouse model of Alzheimer’s disease reveals sex-dependent dysregulations

Muhammad Ali
Pierre Garcia
Enrico Glaab
ResearchOpen Access07 Mar 2024
Cell Death Discovery

Volume: 10, P: 1-19
Neuronal AMP-activated protein kinase hyper-activation induces synaptic loss by an autophagy-mediated process

Manon Domise
Florent Sauvé
Valérie Vingtdeux
ResearchOpen Access04 Mar 2019
Cell Death & Disease

Volume: 10, P: 1-15
The Chemokine MIP-1α/CCL3 impairs mouse hippocampal synaptic transmission, plasticity and memory

Elodie Marciniak
Emilie Faivre
Sandrine Humez
ResearchOpen Access29 Oct 2015
Scientific Reports

Volume: 5, P: 1-11
AMP-activated protein kinase modulates tau phosphorylation and tau pathology in vivo

Manon Domise
Sébastien Didier
Valérie Vingtdeux
ResearchOpen Access27 May 2016
Scientific Reports

Volume: 6, P: 1-12
Alternative promoter usage generates novel shorter MAPT mRNA transcripts in Alzheimer’s disease and progressive supranuclear palsy brains

Vincent Huin
Luc Buée
Claire-Marie Dhaenens
ResearchOpen Access03 Oct 2017
Scientific Reports

Volume: 7, P: 1-10
Loss of Tau protein affects the structure, transcription and repair of neuronal pericentromeric heterochromatin

Zeyni Mansuroglu
Houda Benhelli-Mokrani
Eliette Bonnefoy
ResearchOpen Access08 Sept 2016
Scientific Reports

Volume: 6, P: 1-16
Chronically stressed or stress-preconditioned neurons fail to maintain stress granule assembly

Tatyana A Shelkovnikova
Pasquale Dimasi
Vladimir L Buchman
ResearchOpen Access11 May 2017
Cell Death & Disease

Volume: 8, P: e2788

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Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1

Inhibition of tau neuronal internalization using anti-tau single domain antibodies

Age-related shift in LTD is dependent on neuronal adenosine A_2A receptors interplay with mGluR5 and NMDA receptors

The caffeine-binding adenosine A_2A receptor induces age-like HPA-axis dysfunction by targeting glucocorticoid receptor function

Reply to: Questioning the cycad theory of Kii ALS–PDC causation

Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats

Tau accumulation in astrocytes of the dentate gyrus induces neuronal dysfunction and memory deficits in Alzheimer’s disease

NLRP3 inflammasome activation drives tau pathology

Upregulation of adenosine A_2A receptor in astrocytes is sufficient to trigger hippocampal multicellular dysfunctions and memory deficits

Role of the Tau N-terminal region in microtubule stabilization revealed by newendogenous truncated forms

Effects of the therapeutic correction of U1 snRNP complex on Alzheimer’s disease

Endemic parkinsonism: clusters, biology and clinical features

The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer’s disease

Single cell transcriptome analysis of the THY-Tau22 mouse model of Alzheimer’s disease reveals sex-dependent dysregulations

Neuronal AMP-activated protein kinase hyper-activation induces synaptic loss by an autophagy-mediated process

The Chemokine MIP-1α/CCL3 impairs mouse hippocampal synaptic transmission, plasticity and memory

AMP-activated protein kinase modulates tau phosphorylation and tau pathology in vivo

Alternative promoter usage generates novel shorter MAPT mRNA transcripts in Alzheimer’s disease and progressive supranuclear palsy brains

Loss of Tau protein affects the structure, transcription and repair of neuronal pericentromeric heterochromatin

Chronically stressed or stress-preconditioned neurons fail to maintain stress granule assembly

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