Abstract

Azadeh Esmaeili*, Michelle Hough, Kimia Davoodi, Sherwin Toluie, Hamidreza Goodarzynejad, Yalda Behbahani, Aryan Esmaeili, William Yong, Georgette Buga

ABSTRACT

Alzheimer’s disease (AD) is the most common cause of cognitive dementia, demonstrated by a progressive decline in cognitive function and memory. AD has no current curative treatments in overcoming the underlying pathology of the disease, although palliative treatments are available. This paper reviews the potential mechanism of the ApoA-I mimetic peptide for the prevention and treatment of cognitive impairment induced by hyperlipidemia and AD. Projected mechanisms suggest the peptide may: 1) reduce inflammation and wall thickness in small arteries and 2) prevent synaptic and neuronal loss induced by immune system response. Considering ‘Western diet’ (42% fat, 0.15% cholesterol)-induced cognitive dysfunction and the underlying pathogenesis of AD, targeting vascular pathology and immune response may prove to be clinically effective in treating AD and hyperlipidemia-induced cognitive dysfunction.