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Start Over Author "Chamoun, Mira" Journal nature communications
4 results on '"Chamoun, Mira"'

1. Author Correction: [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease

Author

Pascoal, Tharick A., Chamoun, Mira, Lax, Elad, Wey, Hsiao-Ying, Shin, Monica, Ng, Kok Pin, Kang, Min Su, Mathotaarachchi, Sulantha, Benedet, Andrea L., Therriault, Joseph, Lussier, Firoza Z., Schroeder, Frederick A., DuBois, Jonathan M., Hightower, Baileigh G., Gilbert, Tonya M., Zürcher, Nicole R., Wang, Changning, Hopewell, Robert, Chakravarty, Mallar, Savard, Melissa, Thomas, Emilie, Mohaddes, Sara, Farzin, Sarah, Salaciak, Alyssa, Tullo, Stephanie, Cuello, A. Claudio, Soucy, Jean-Paul, Massarweh, Gassan, Hwang, Heungsun, Kobayashi, Eliane, Hyman, Bradley T., Dickerson, Bradford C., Guiot, Marie-Christine, Szyf, Moshe, Gauthier, Serge, Hooker, Jacob M., and Rosa-Neto, Pedro

Published
2022
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2. [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease

Author

Pascoal, Tharick A., Chamoun, Mira, Lax, Elad, Wey, Hsiao-Ying, Shin, Monica, Ng, Kok Pin, Kang, Min Su, Mathotaarachchi, Sulantha, Benedet, Andrea L., Therriault, Joseph, Lussier, Firoza Z., Schroeder, Frederick A., DuBois, Jonathan M., Hightower, Baileigh G., Gilbert, Tonya M., Zürcher, Nicole R., Wang, Changning, Hopewell, Robert, Chakravarty, Mallar, Savard, Melissa, Thomas, Emilie, Mohaddes, Sara, Farzin, Sarah, Salaciak, Alyssa, Tullo, Stephanie, Cuello, A. Claudio, Soucy, Jean-Paul, Massarweh, Gassan, Hwang, Heungsun, Kobayashi, Eliane, Hyman, Bradley T., Dickerson, Bradford C., Guiot, Marie-Christine, Szyf, Moshe, Gauthier, Serge, Hooker, Jacob M., and Rosa-Neto, Pedro

Published
2022
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4. [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer's disease.

Author

Pascoal, Tharick A., Chamoun, Mira, Lax, Elad, Wey, Hsiao-Ying, Shin, Monica, Ng, Kok Pin, Kang, Min Su, Mathotaarachchi, Sulantha, Benedet, Andrea L., Therriault, Joseph, Lussier, Firoza Z., Schroeder, Frederick A., DuBois, Jonathan M., Hightower, Baileigh G., Gilbert, Tonya M., Zürcher, Nicole R., Wang, Changning, Hopewell, Robert, Chakravarty, Mallar, and Savard, Melissa

Subjects
ALZHEIMER'S disease, TAU proteins, POSITRON emission tomography, HISTONES, HISTONE deacetylase, CEREBRAL atrophy, PATIENT-ventilator dyssynchrony, FORENSIC pathology
Abstract

Alzheimer's disease (AD) is characterized by the brain accumulation of amyloid-β and tau proteins. A growing body of literature suggests that epigenetic dysregulations play a role in the interplay of hallmark proteinopathies with neurodegeneration and cognitive impairment. Here, we aim to characterize an epigenetic dysregulation associated with the brain deposition of amyloid-β and tau proteins. Using positron emission tomography (PET) tracers selective for amyloid-β, tau, and class I histone deacetylase (HDAC I isoforms 1–3), we find that HDAC I levels are reduced in patients with AD. HDAC I PET reduction is associated with elevated amyloid-β PET and tau PET concentrations. Notably, HDAC I reduction mediates the deleterious effects of amyloid-β and tau on brain atrophy and cognitive impairment. HDAC I PET reduction is associated with 2-year longitudinal neurodegeneration and cognitive decline. We also find HDAC I reduction in the postmortem brain tissue of patients with AD and in a transgenic rat model expressing human amyloid-β plus tau pathology in the same brain regions identified in vivo using PET. These observations highlight HDAC I reduction as an element associated with AD pathophysiology. The link between amyloid and tau proteins with Alzheimer's disease progression remains unclear. Here, the authors propose HDACs I downregulation as an element linking the deleterious effects of brain proteinopathies with disease progression. [ABSTRACT FROM AUTHOR]

Published
2022
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