Role of metabolism in neurodegenerative disorders

• Published in: Metabolism, clinical and experimental Vol. 65; no. 9; pp. 1376 - 1390
• Main Authors: Procaccini, Claudio, Santopaolo, Marianna, Faicchia, Deriggio, Colamatteo, Alessandra, Formisano, Luigi, de Candia, Paola, Galgani, Mario, De Rosa, Veronica, Matarese, Giuseppe
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2016
• Subjects: Alzheimer's disease; Endocrinology & Metabolism; Energy Metabolism - genetics; Hormones - metabolism; Humans; Huntington's diseases; Metabolism; Multiple sclerosis; Neurodegenerative Diseases - genetics; Neurodegenerative Diseases - metabolism; Parkinson's disease; Receptor Cross-Talk; Type 2 diabetes; APP; Multiple sclerosis; Parkinson's disease; T1D; neuropeptide Y; leptin receptor b; nitic oxide; IGFBP; Aβ; db/ db; experimental autoimmune encephalomyelitis; Huntington's diseases; PI3K; mTOR; Janus kinase; brain-derived neurotrophic factor; Alzheimer's disease; NFT; obesity; β-amyloid; caloric restriction; MS; body mass index; T2D; relapsing–remitting multiple sclerosis; EAE; IR; IGF-1; myelin basic protein; MAPK; Insulin receptor substrate; suppressor of cytokine signaling-3; Extracellular-signal-regulated kinases; AMPK; metabolism; leptin-receptor-deficient; ERK; RRMS; NO; Signal transducer and activator of transcription; neurofibrillary tangles; Insulin-like growth factor-1; CNS; IRS; AMP-activated protein kinase; Phosphoinositide 3-kinase; mammalian target of rapamycin; ob/ ob; CREB; cAMP response element-binding protein; amyloid precursor protein; PLP; huntingtin; NPY; UCP2; LepRb; central nervous sytem; MBP; Insulin receptor; Adenosine triphosphate; BMI; type 1 diabetes; proteolipid protein; BDNF; Insulin growth factor binding protein; Mitogen-activated protein kinase; htt; SOCS-3; Uncoupling Protein-2; CR; STAT; JAK; leptin-deficient; ATP; db/db; ob/ob; Metabolism
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2016.05.018

Abstract Along with the increase in life expectancy over the last century, the prevalence of age-related disorders, such as neurodegenerative diseases continues to rise. This is the case of Alzheimer's, Parkinson's, Huntington's diseases and Multiple sclerosis, which are chronic disorders characterized by neuronal loss in motor, sensory or cognitive systems. Accumulating evidence has suggested the presence of a strong correlation between metabolic changes and neurodegeneration. Indeed epidemiologic studies have shown strong associations between obesity, metabolic dysfunction, and neurodegeneration, while animal models have provided insights into the complex relationships between these conditions. In this context, hormones such as leptin, ghrelin, insulin and IGF-1 seem to play a key role in the regulation of neuronal damage, toxic insults and several other neurodegenerative processes. This review aims to presenting the most recent evidence supporting the crosstalk linking energy metabolism and neurodegeneration, and will focus on metabolic manipulation as a possible therapeutic tool in the prevention and treatment of neurodegenerative diseases.