A Review on Therapeutic Effects of Humanin, a New Peptide in Treatment of Alzheimer Disease abstract
Introduction: Alzheimer’s disease is the most prevalent neurological disease with dementia. AD-related dementia is caused by death and dysfunction of neurons involved in cognitive function. It has been generally believed that increased levels of toxic amyloid-betas are linked to the occurrence of neuronal death as well as dysfunction. Consequently, lowering levels of toxic Aβs in the brain is considered to be central for therapy of AD. Humanin is a mitochondrial-derived peptide with 24 aminoacids (MAPRGFSCLLLLTSEIDLPVKRRA), Its expression in humans has been shown to decrease with age, which suggests a possible causal relationship between decreased HN and the onset of old age diseases like AD and type 2 diabetes. HN and its derivatives are peptides known for their neuroprotective effects against Alzheimer’s disease.Thus the aim of this study is to review on ability of humanin that has therapeutic effect on amyloid accumulation in AD and suppresses neuronal cell death induced by Aβ. Materials and methods: We searched Pubmed, Scopus, Ovid and Proquest with the terms such as: humanin peptide, Alzheimer’s disease and neuroprotective factor. The search covered 2001 until 2014. Among 50 searched articles, 40 references were studied. Results: A series of experiments using mouse AD models established the efficacy of HN against AD. HN suppresses neuronal cell death caused by AD including both amyloid-betas peptides and familial AD-causative genes. An intracellular anti-apoptotic mechanism has been demonstrated, revealing the capacity of HN to bind the BAX protein family. Cerebrovascular smooth muscle cells are also protected from Aβ toxicity by HN, suggesting that HN affects both neuronal and non-neuronal cells when they are exposed to AD-related cytotoxicity. HN can be viewed as drug candidates for neuronal death suppression therapy in AD.Conclusion: Since its discovery, HN has been demonstrated to offer beneficial effects in many diseases, many of which are age-related. Gain and loss of function models are necessary to fill the gaps in our current knowledge and enhance our understanding of the physiological role of this peptide in various diseases.