Ammaarah Khatri

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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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 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

The metabolism of human soluble amyloid precursor protein isoforms is quantifiable by a stable isotope labeling-tandem mass spectrometry method

Justyna A. Dobrowolska Zakaria, Randall J. Bateman, Monika Łysakowska, Ammaarah Khatri et autres

Evidence suggests that β-secretase (BACE1), which cleaves Amyloid Precursor Protein (APP) to form sAPPβ and amyloid-β, is elevated in Alzheimer's disease (AD) brains and biofluids and, thus, BACE1 is a therapeutic target for this devastating disease. The direct product of BACE1 cleavage …

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

Alexis R. Demonbreun, Elena Bogdanovic, Lauren A. Vaught, Nina L. Reiser et autres

Membrane instability and disruption underlie myriad acute and chronic disorders. Anxa6 encodes the membrane-associated protein annexin A6 and was identified as a genetic modifier of muscle repair and muscular dystrophy. To evaluate annexin A6's role in membrane repair in vivo, we inserted …

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A Method For The Quantitation Of The Metabolism Of Soluble Amyloid Precursor Protein Isoforms Using A Stable Isotope Labeling Kinetics Approach Paired With Tandem Mass Spectrometry

Justyna A. Dobrowolska Zakaria, Randall J. Bateman, Monika Łysakowska, Ammaarah Khatri et autres

Abstract Evidence suggests that β-secretase (BACE1), which cleaves Amyloid Precursor Protein (APP) to form sAPPβ and Aβ, is elevated in AD brains and biofluids and, thus, BACE1 is a therapeutic target for this devastating disease. The direct product of BACE1 cleavage of …

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

Katherine R. Sadleir, Jelena Popović, Ammaarah Khatri, Robert Vassar

Dysregulation of calcium homeostasis has been hypothesized to play a role in Alzheimer's disease (AD) pathogenesis. Increased calcium levels can impair axonal transport, disrupt synaptic transmission, and ultimately lead to cell death. Given the potential role of calcium dyshomeostasis in AD, there …

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