Poster Session II - Abstract # 20

Increased Plasma Acylated Ghrelin is a Potential Biomarker for Alzheimer's Disease

Jing Tian¹, Russell Swerdlow³, Heng Du^1,2,3

¹Department of Pharmacology & Toxicology, ²Higuchi Biosciences Center, University of Kansas, Lawrence, KS, USA;  ³University of Kansas Medical Center, University of Kansas, Kansas City, KS, USA

Characterized by progressive cognitive decline, Alzheimer’s disease (AD) is the most common type of dementia attacking the aged population. The detailed etiopathogenesis of AD, especially of its sporadic type remains largely unknown; and reliable approaches for early diagnosis are still lacking. Ghrelin is a brain-gut peptide that involves in the regulation of hippocampal synaptic activity. Previous studies showed inactivation of ghrelin receptor in the hippocampi from the patients, which underlies AD-related cognitive impairment. Here, we found a paradoxical elevation in plasma acyl ghrelin, the bioactive form of ghrelin in a KUMC AD cohort. The ratio of acyl ghrelin to its endogenous antagonist, liver-expressed antimicrobial peptide 2 (LEAP2) was in a negative relationship with the severity of cognitive dysfunction in patients. Receiver operating characteristic (ROC) curves further indicate the diagnostic capability of acyl ghrelin levels and acyl ghrelin/LEAP2 ratio. Therefore, circulating acyl ghrelin and acyl ghrelin/LEAP2 ratio may constitute potential reliable blood-based biomarkers for the diagnosis of AD. Moreover, the results in combination with incapacitation of ghrelin receptor add credit to a hypothesis of “ghrelin resistance” in the development of AD.