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Connections between ApoE, sleep, and Aβ and tau pathologies in Alzheimer's disease

The Journal of clinical investigation, 2023-07, Vol.133 (14)

2023

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Oral nimodipine treatment has no effect on amyloid pathology or neuritic dystrophy in the 5XFAD mouse model of amyloidosis

PloS one, 2022-02, Vol.17 (2), p.e0263332-e0263332

2022

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Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis

Neuron (Cambridge, Mass.), 2008-12, Vol.60 (6), p.988-1009

2008

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Aberrant glial activation and synaptic defects in CaMKIIα-iCre and nestin-Cre transgenic mouse models

Scientific reports, 2022-12, Vol.12 (1), p.22099-22099, Article 22099

2022

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Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging

Nature communications, 2024-01, Vol.15 (1), p.264-264, Article 264

2024

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Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease

PloS one, 2014-07, Vol.9 (7), p.e101643

2014

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ER stress is not elevated in the 5XFAD mouse model of Alzheimer's disease

The Journal of biological chemistry, 2018-11, Vol.293 (48), p.18434-18443

2018

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Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer’s disease

Acta neuropathologica, 2016-08, Vol.132 (2), p.235-256

2016

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The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's disease

Nature (London), 2020-10, Vol.586 (7831), p.735-740

2020

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A conserved annexin A6–mediated membrane repair mechanism in muscle, heart, and nerve

JCI insight, 2022-07, Vol.7 (14)

2022

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The Alzheimer’s β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques

Acta neuropathologica, 2013-09, Vol.126 (3), p.329-352

2013

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RPS23RG1 May Prevent Ubiquitin-Proteosomal Degradation of Postsynaptic Densities-93 and -95 to Protect Synaptic Function: Implications for Alzheimer’s Disease

Biological psychiatry (1969), 2019-08, Vol.86 (3), p.164-166

2019

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Cdk5 protein inhibition and Aβ42 increase BACE1 protein level in primary neurons by a post-transcriptional mechanism: implications of CDK5 as a therapeutic target for Alzheimer disease

The Journal of biological chemistry, 2012-03, Vol.287 (10), p.7224-7235

2012

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Elevated Aβ42 in aged, non-demented individuals with cerebral atherosclerosis

Current Alzheimer research, 2013-10, Vol.10 (8), p.785

2013

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Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level

Molecular neurodegeneration, 2015-01, Vol.10 (1), p.1-1, Article 1

2015

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Modeling genetic diversity in Alzheimer's disease

Lab animal, 2019-03, Vol.48 (3), p.87

2019

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Cdk5 Protein Inhibition and Aβ42 Increase BACE1 Protein Level in Primary Neurons by a Post-transcriptional Mechanism

The Journal of biological chemistry, 2012-03, Vol.287 (10), p.7224-7235

2012

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Connections between ApoE, sleep, and A[beta] and tau pathologies in Alzheimer's disease

The Journal of clinical investigation, 2023-07, Vol.133 (14)

2023

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Dimebon alters hippocampal amyloid pathology in 3xTg-AD mice

International journal of physiology, pathophysiology and pharmacology, 2012, Vol.4 (3), p.115-127

2012

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MOLECULAR MECHANISMS OF THE ALZHEIMER’S RISK GENE UNC5C IN NEURONAL DEATH

Alzheimer's & dementia, 2018-07, Vol.14 (7), p.P340-P340

2018

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P1‐163: MOLECULAR MECHANISMS OF THE ALZHEIMER'S RISK GENE UNC5C IN NEURONAL DEATH

Alzheimer's & dementia, 2018-07, Vol.14 (7S_Part_6), p.P340-P340

2018

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Innate immunity protein IFITM3 modulates γ-secretase in Alzheimer disease

Nature (London), 2020-09, Vol.586 (7831), p.735-740

2020

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Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased A[beta] generation in Alzheimer's disease

Acta neuropathologica, 2016-08, Vol.132 (2), p.235

2016

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Genetic Inhibition of Phosphorylation of the Translation Initiation Factor eIF2[alpha] Does Not Block A[beta]-Dependent Elevation of BACE1 and APP Levels or Reduce Amyloid Pathology in a Mouse Model of Alzheimer's Disease

PloS one, 2014-07, Vol.9 (7)

2014

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Erratum to: the Alzheimer's [beta]-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques

Acta neuropathologica, 2013-10, Vol.126 (4), p.623

2013

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Connections between ApoE, sleep, and Aβ and tau pathologies in Alzheimer's disease

Oral nimodipine treatment has no effect on amyloid pathology or neuritic dystrophy in the 5XFAD mouse model of amyloidosis

Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis

Aberrant glial activation and synaptic defects in CaMKIIα-iCre and nestin-Cre transgenic mouse models

Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging

Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease

ER stress is not elevated in the 5XFAD mouse model of Alzheimer's disease

Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer’s disease

The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's disease

A conserved annexin A6–mediated membrane repair mechanism in muscle, heart, and nerve

The Alzheimer’s β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques

RPS23RG1 May Prevent Ubiquitin-Proteosomal Degradation of Postsynaptic Densities-93 and -95 to Protect Synaptic Function: Implications for Alzheimer’s Disease

Cdk5 protein inhibition and Aβ42 increase BACE1 protein level in primary neurons by a post-transcriptional mechanism: implications of CDK5 as a therapeutic target for Alzheimer disease

Elevated Aβ42 in aged, non-demented individuals with cerebral atherosclerosis

Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level

Modeling genetic diversity in Alzheimer's disease

Cdk5 Protein Inhibition and Aβ42 Increase BACE1 Protein Level in Primary Neurons by a Post-transcriptional Mechanism

Connections between ApoE, sleep, and A[beta] and tau pathologies in Alzheimer's disease

Dimebon alters hippocampal amyloid pathology in 3xTg-AD mice

MOLECULAR MECHANISMS OF THE ALZHEIMER’S RISK GENE UNC5C IN NEURONAL DEATH

P1‐163: MOLECULAR MECHANISMS OF THE ALZHEIMER'S RISK GENE UNC5C IN NEURONAL DEATH

Innate immunity protein IFITM3 modulates γ-secretase in Alzheimer disease

Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased A[beta] generation in Alzheimer's disease

Genetic Inhibition of Phosphorylation of the Translation Initiation Factor eIF2[alpha] Does Not Block A[beta]-Dependent Elevation of BACE1 and APP Levels or Reduce Amyloid Pathology in a Mouse Model of Alzheimer's Disease

Erratum to: the Alzheimer's [beta]-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques

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