Katherine R. Sadleir

Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer’s disease model mice

Katherine R. Sadleir, Karen P Gomez, Sidhanth Chandra, Makenna Ley et autres

Background: The hallmark lesions of the Alzheimer's disease (AD) brain are amyloid plaques consisting of the β-amyloid protein and neurofibrillary tangles comprised of hyperphosphorylated, aggregated tau protein, which both cause neuronal dysfunction and loss. One goal of neuroprotective therapies is to maintain …

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The UNC5C T835M mutation associated with Alzheimer’s disease leads to neurodegeneration involving oxidative stress and hippocampal atrophy in aged mice

Devi Krishna Priya Karunakaran, Makenna Ley, Ammaarah Khatri, Katherine R. Sadleir et autres

Abstract Alzheimer’s disease (AD) is characterized by amyloid plaques, neurofibrillary tangles, and synaptic and neuronal loss. Recently, a rare autosomal dominant coding mutation, T835M, in the Un-coordinated 5c (UNC5C) netrin receptor gene was segregated with late-onset AD (LOAD). Overexpression of T835M in …

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Annexin A6 membrane repair protein protects against amyloid-induced dystrophic neurites and tau phosphorylation in Alzheimer’s disease model mice

Katherine R. Sadleir, Karen Gómez, A. Edwards, Makenna Ley et autres

In Alzheimer's disease, accumulation of amyloid-β (Aβ) peptide is thought to cause formation of neurofibrillary tangles composed of hyperphosphorylated tau protein, which correlates with neuronal loss and cognitive impairment, but the mechanism linking Aβ and tau pathologies is unknown. Dystrophic neurites, which …

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The gut microbiome controls reactive astrocytosis during Aβ amyloidosis via propionate-mediated regulation of IL-17

Sidhanth Chandra, Jelena Popović, Naveen Kumar Singhal, Hemraj B. Dodiya et autres

Accumulating evidence implicates the gut microbiome (GMB) in the pathogenesis and progression of Alzheimer's disease (AD). We recently showed that the GMB regulates reactive astrocytosis and Aβ plaque accumulation in a male APPPS1-21 AD mouse model. Yet, the mechanism(s) by which GMB …

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The UNC5C T835M mutation associated with Alzheimer’s disease leads to neurodegeneration involving oxidative stress and hippocampal atrophy in aged mice

Devi Krishna Priya Karunakaran, Makenna Ley, Ammaarah Khatri, Katherine R. Sadleir et autres

Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice

Andrew Octavian Sasmita, Constanze Depp, T. I. Nazarenko, Ting Sun et autres

Abstract Amyloid-β (Aβ) is thought to be neuronally derived in Alzheimer’s disease (AD). However, transcripts of amyloid precursor protein ( APP ) and amyloidogenic enzymes are equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion of Bace1 in a humanized knock-in AD model, …

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

Bidur Paudel, Si‐Yeon Jeong, Carolina Pena Martinez, Alexis Rickman et autres

Alzheimer's disease (AD) is characterized by progressive neurodegeneration, but the specific events that cause cell death remain poorly understood. Death Induced by Survival gene Elimination (DISE) is a cell death mechanism mediated by short (s) RNAs acting through the RNA-induced silencing complex …

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Oligodendrocytes and neurons contribute to amyloid-β deposition in Alzheimer’s disease

Andrew Octavian Sasmita, Constanze Depp, T. I. Nazarenko, Ting Sun et autres

In Alzheimer’s disease (AD), amyloid-β (Aβ) is thought to be of neuronal origin. However, in single-cell RNAseq datasets from mouse and human, we found transcripts of amyloid precursor protein (APP) and the amyloidogenic-processing machinery equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion …

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

Katherine R. Sadleir, Robert Vassar

In this issue of the JCI, Wang and colleagues investigate the relationship between sleep disturbances, an environmental risk factor for Alzheimer's disease (AD), and the apolipoprotein 4 (APOEε4) allele, a strong genetic risk factor for AD. The authors subjected an amyloid mouse …

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The gut microbiome regulates astrocyte reaction to Aβ amyloidosis through microglial dependent and independent mechanisms

Sidhanth Chandra, Antonio Di Meco, Hemraj B. Dodiya, Jelena Popović et autres

BACKGROUND: Previous studies show that antibiotic-mediated (abx) alteration of the gut microbiome (GMB) results in a reduction of amyloid beta (Aβ) plaques and proinflammatory microglial phenotype in male APPPS1-21 mice. However, the effect of GMB perturbation on astrocyte phenotypes and microglial-astrocyte communication …

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

Alia O. Alia, Sohee Jeon, Jelena Popović, Miranda A. Salvo et autres

Current scientific research is driven by the ability to manipulate gene expression by utilizing the Cre/loxP system in transgenic mouse models. However, artifacts in Cre-driver mouse lines that introduce undesired effects and confound results are increasingly being reported. Here, we show aberrant …

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

Alia O. Alia, Jelena Popović, Miranda A. Salvo, Katherine R. Sadleir et autres

Abstract Current scientific research is driven by the ability to manipulate gene expression by utilizing the Cre/loxP system in transgenic mouse models. However, artifacts in Cre-driver mouse lines that introduce undesired effects and confound results are increasingly being reported. Here, we show …

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