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Fullerene C60 Prevents Neurotoxicity Induced by Intrahippocampal Microinjection of Amyloid-β Peptide

http://www.ingentaconnect.com/content/asp/jnn/2012/00000012/00000001/art00011?token=004d1178c39412f415d763f256f706e7b5f2473386f2530482972715a614f6d4e227a0ab6fac9

Authors: Makarova, E.G.; Gordon, R.Y.a.; Podolski, I.Y.a.

Source: Journal of Nanoscience and Nanotechnology, Volume 12, Number 1, January 2012 , pp. 119-126(8)

Publisher: American Scientific Publishers

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Abstract:

The dynamics of the state of hippocampal pyramidal neurons after intrahippocampal microinjections of (1) amyloid-β25-35 (1.6 nmol/1 μl), (2) an aqueous molecule-colloidal solution of C60 (0.46 nmol/1 μl) and (3) an aqueous molecule-colloidal solution of C60 before amyloid-β25-35 administration were analysed in rats. This model allowed us to study the role of amyloid-β25-35 in the pathogenesis of Alzheimer's disease and to test anti-amyloid substances. Methods of fluorescent (acridine orange) and brightfield (cresyl violet and immunohistochemistry) microscopy were used. Acridine orange staining indicated changes in protein synthesis intensity due to alterations in the rRNA state of neuron ribosomes. One day after administration of amyloid-β25-35, the intensity of protein synthesis in the population of morphologically intact cells decreased by 45%. By day 14, degeneration occurred in the majority of pyramidal cells, and amyloid-β25-35 deposits were observed in the neuronal cytoplasm. In necrotic cells, acridine orange staining of the cytoplasm was drastically increased as a result of RNA degradation rather than due to an increase in protein synthesis. Because amyloid-β25-35 administration provoked oxidative stress, we assumed that an aqueous molecule-colloidal solution of C60 administered before amyloid-β25-35 prevented protein synthesis changes on day 1, while acting as an antioxidant, and by day 14 it inhibited neurodegeneration and amyloid-β25-35 accumulation. Based on the data that an aqueous molecule-colloidal solution of C60 prevented amyloid-β25-35 aggregation in in vitro experiments and based on our present evidence on the antitoxicity of an aqueous molecule-colloidal solution of C60, we suggest that functionalised C60 prevents/diminishes amyloid-β25-35 aggregation in vivo as well. Thus, an aqueous molecule-colloidal solution of C60 administered at a low concentration before amyloid-β25-35, prevented disturbances in protein synthesis, neurodegeneration and formation amyloid-β25-35 deposits in hippocampal pyramidal neurons in vivo. This evidence gives promise that functionalised C60 can be used to develop anti-amyloid drugs combining antioxidant and anti-aggregative properties.

Keywords: AQUEOUS MOLECULE-COLLOIDAL SOLUTION OF C60; C60 HYDRATED FULLERENE; ANTI-AMYLOID DRUGS; ALZHEIMER'S DISEASE; NEURODEGENERATION; PROTEIN SYNTHESIS; PYRAMIDAL NEURONS; HIPPOCAMPAL CA1 FIELD

Document Type: Research article

DOI: http://dx.doi.org/10.1166/jnn.2012.5709

Publication date: 2012-01-01

Thanks for your kind assistance.

I suggest you get in touch with Dr Grigoriy Andrievsky in Kharkiv Ukraine, who has done work in this area. He speaks English too. His email is [email protected] Good Luck

Ya might want to try TEMPOL or PBN