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Article

Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer’s Disease

1
Field Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mt. Pleasant, MI 48859, USA
2
Department of Psychology, Central Michigan University, Mt. Pleasant, MI 48859, USA
3
Program in Neuroscience, Central Michigan University, Mt. Pleasant, MI 48859, USA
4
Field Neurosciences Institute, Ascension St. Mary, Saginaw, MI 48604, USA
5
College of Health and Human Services, Saginaw Valley State University, Saginaw, MI 48604, USA
6
Department of Biology, Eckerd College, St. Petersburg, FL 33711, USA
7
Department of Chemistry, Eckerd College, St. Petersburg, FL 33711, USA
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(18), 6664; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186664
Received: 28 July 2020 / Revised: 7 September 2020 / Accepted: 9 September 2020 / Published: 11 September 2020
(This article belongs to the Collection Neuroinflammatory Processes in Neurodegenerative Diseases)
Alzheimer’s disease (AD) is characterized by amyloid (Aβ) aggregation, hyperphosphorylated tau, neuroinflammation, and severe memory deficits. Reports that certain boronic compounds can reduce amyloid accumulation and neuroinflammation prompted us to compare trans-2-phenyl-vinyl-boronic-acid-MIDA-ester (TPVA) and trans-beta-styryl-boronic-acid (TBSA) as treatments of deficits in in vitro and in vivo models of AD. We hypothesized that these compounds would reduce neuropathological deficits in cell-culture and animal models of AD. Using a dot-blot assay and cultured N2a cells, we observed that TBSA inhibited Aβ42 aggregation and increased cell survival more effectively than did TPVA. These TBSA-induced benefits were extended to C. elegans expressing Aβ42 and to the 5xFAD mouse model of AD. Oral administration of 0.5 mg/kg dose of TBSA or an equivalent amount of methylcellulose vehicle to groups of six- and 12-month-old 5xFAD or wild-type mice over a two-month period prevented recognition- and spatial-memory deficits in the novel-object recognition and Morris-water-maze memory tasks, respectively, and reduced the number of pyknotic and degenerated cells, Aβ plaques, and GFAP and Iba-1 immunoreactivity in the hippocampus and cortex of these mice. These findings indicate that TBSA exerts neuroprotective properties by decreasing amyloid plaque burden and neuroinflammation, thereby preventing neuronal death and preserving memory function in the 5xFAD mice. View Full-Text
Keywords: Alzheimer’s disease; amyloid beta protein; neurodegeneration; boron compound; neuroinflammation; amyloid plaque; C. elegans Alzheimer’s disease; amyloid beta protein; neurodegeneration; boron compound; neuroinflammation; amyloid plaque; C. elegans
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MDPI and ACS Style

Maiti, P.; Manna, J.; Burch, Z.N.; Flaherty, D.B.; Larkin, J.D.; Dunbar, G.L. Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer’s Disease. Int. J. Mol. Sci. 2020, 21, 6664. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186664

AMA Style

Maiti P, Manna J, Burch ZN, Flaherty DB, Larkin JD, Dunbar GL. Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer’s Disease. International Journal of Molecular Sciences. 2020; 21(18):6664. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186664

Chicago/Turabian Style

Maiti, Panchanan; Manna, Jayeeta; Burch, Zoe N.; Flaherty, Denise B.; Larkin, Joseph D.; Dunbar, Gary L. 2020. "Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer’s Disease" Int. J. Mol. Sci. 21, no. 18: 6664. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186664

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