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Moderate consumption of beer is known to be beneficial for health. Thus, antioxidant, likely taste, and aroma properties of antho-beers made from purple wheat grain (antho-grain) were evaluated. The 2,2-diphenyl-1-picryhydrazyl free radical (DPPH*) scavenging activity, total phenolic content (TPC), oxygen radical absorbance capacity (ORAC), and phenolic acid compositions of antho-bran were also investigated. DPPH* scavenging activity at 60 min was 50.6-59.9% for control and antho-beer extracts, 15.0-54.1% for antho-bran extracts and hydrolysates. The TPC ranged from 410 to 609 mg/L, from 84 to 95 mg/L, and from 2473 to 7634 mg/kg for control (from barley malt) and antho-beer original samples, control and antho-beer extracts, and antho-bran extracts and hydrolysates, respectively. The corresponding ORAC values were 3050-4181 mg/L, 2961-3184 mg/L, and 74-213 g/kg, respectively. The major known phenolic acids comprised four types in control beer, five types in antho-beers, and seven types in antho-bran hydrolysates. Total anthocyanin content of antho-bran was up to 1160 mg/kg. Differences in likely taste and aroma were found between control and antho-beers by using electronic tongue and nose methods. Brewing materials had an effect on the antioxidant, likely taste, and aroma properties of beers; however, antho-grain may have potential as a novel brewing material.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological changes, including the deposition of amyloid-beta (Aβ) peptide. Aged monkeys have proven to be invaluable in the study of AD, as their brains naturally develop amyloid plaques similar to those in AD brains. However, spontaneous development of AD-like pathologies in aged monkeys is time-consuming, often taking several years. Here, we created an experimentally induced AD model in middle-aged (16-17 years) rhesus monkeys by intracranial injection of Aβ42 and thiorphan, an inhibitor of neprilysin that is responsible for Aβ clearance. The working memory capacity of the monkeys in a delayed-response task was little affected following the delivery of Aβ42 and thiorphan. However, the administration of Aβ42 and thiorphan resulted in a significant intracellular accumulation of Aβ in the neurons of the basal ganglia, the cortex, and the hippocampus, accompanied by neuronal atrophy and loss. Moreover, immunohistochemistry revealed a degeneration of choline acetyltransferase-positive cholinergic neurons and an increase of glial fibrillary acidic protein-positive astrocytes. In conclusion, our data demonstrate a primate model of AD generated by combined infusion of Aβ42 and thiorphan, which duplicates a subset of neuropathological changes in AD brains, thereby having implications in the elucidation of this disease.

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