The proof-of-concept of ASS234: Peripherally administered ASS234 enters the central nervous system and reduces pathology in a male mouse model of Alzheimer disease
Author(s) -
Mari Paz SerranoRegal,
Raquel Herrero-Labrador,
Hunter S. Futch,
Julia Serrano,
Alejandro Romero,
Ana Patricia Fernández,
Abdelouahid Samadi,
Mercedes Unzeta,
José MarcoContelles,
Ricardo Martı́nez-Murillo
Publication year - 2016
Publication title -
journal of psychiatry and neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 99
eISSN - 1488-2434
pISSN - 1180-4882
DOI - 10.1503/jpn.150209
Subject(s) - gliosis , alzheimer's disease , donepezil , hippocampus , pharmacology , cholinergic , in vivo , genetically modified mouse , monoamine oxidase , pathology , medicine , biology , dementia , disease , transgene , biochemistry , gene , enzyme , microbiology and biotechnology
The heterogeneity of Alzheimer disease requires the development of multitarget drugs for treating the symptoms of the disease and its progression. Both cholinergic and monoamine oxidase dysfunctions are involved in the pathological process. Thus, we hypothesized that the development of therapies focused on these targets might be effective. We have developed and assessed a new product, coded ASS234, a multipotent acetyl and butyrylcholinesterase/monoamine oxidase A-B inhibitor with a potent inhibitory effect on amyloid-β aggregation as well as antioxidant and antiapoptotic properties. But there is a need to reliably correlate in vitro and in vivo drug release data.
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