Monascus purpureus NTU 568 fermented product improves memory and learning ability in rats with aluminium-induced Alzheimer's disease

• ANKASCIN 568 plus intake ameliorated cognitive dysfunction in Alzheimer's disease.
• Aβ1–40 and Aβ1–42 levels reduced in Alzheimer's disease rats fed ANKASCIN 568 plus.
• ANKASCIN 568 plus decreased acetylcholinesterase activity and phosphorylated tau protein levels.
• ANKASCIN 568 plus provided neuroprotection by reducing oxidative stress.
• ANKASCIN 568 plus significantly reduced amyloid precursor protein expression.

Oxidative stress and neuroinflammation induced by accumulation of amyloid β (Aβ) and phosphorylated tau protein (p-tau) are the main causes of Alzheimer's disease (AD). We examined the effects of Monascus purpureus NTU 568 fermented product (ANKASCIN 568 plus) in the model of Sprague–Dawley rats via oral garage to induce AD pathology which received aluminium chloride on a daily basis. ANKASCIN 568 plus mitigated cognitive impairment in behavioural tests, reduced oxidative stress in the brain, reversed aluminium-induced AD brain pathology including accumulation of Aβ, p-tau, and amyloid precursor protein; elevated acetylcholinesterase activity, and altered biomarker levels in the cerebrospinal fluid. ANKASCIN 568 plus showed a significant improvement relative to Aricept, an approved drug for AD, in several parameters. Thus, by suppressing free radical generation and activating antioxidant enzymes, ANKASCIN 568 plus can reduce oxidative stress and ameliorate AD pathology, thus protecting rats against aluminium-induced memory and learning deficits.