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Article type: Short Communication
Authors: Miller, Morgan R. | Lariviere, Lavender | Pagnier, Guillaume J. | Aygar, Sema | Wieckiewicz, Natalia | Maesako, Masato | Bacskai, Brian J. | Kastanenka, Ksenia V.; *
Affiliations: [a] Department of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
Correspondence: [*] Correspondence to: Ksenia V. Kastanenka, MassGeneral Institute of Neurodegenerative Diseases, 114 16th St. Charlestown, MA, 02129, USA. E-mail: kkastanenka@mgh.harvard.edu.
Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disease with limited therapeutic strategies. NB-02 is a novel botanical drug that has shown promise as a protective and therapeutic treatment for AD in an APP/PS1 preclinical mouse model. In this paper, we investigate the underlying mechanisms by which NB-02 provides these therapeutic advantages using in vitro neuron-astrocyte co-cultures. Pretreatment with NB-02 prevented pathological calcium elevations in neurons and astrocytes after application of toxic soluble amyloid-β (Aβ) oligomers. NB-02 also prevented cell death associated with the addition of soluble Aβ oligomers suggesting NB-02 is effective at protecting both neurons and astrocytes from Aβ-mediated damage.
Keywords: Alzheimer’s disease, amyloid, astrocyte, calcium, DA-9803, NB-02, neuron, oligomer, therapy
DOI: 10.3233/JAD-231387
Journal: Journal of Alzheimer's Disease, vol. 99, no. 2, pp. 477-483, 2024
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