Genes and primary headaches: discovering new potential therapeutic targets

Genetic studies have clearly shown that primary headaches (migraine, tension-type headache and cluster headache) are multifactorial disorders characterized by a complex interaction between different genes and environmental factors. Genetic association studies have highlighted a potential role in the etiopathogenesis of these disorders for several genes related to vascular, neuronal and neuroendocrine functions. A potential role as a therapeutic target is now emerging for some of these genes. The main purpose of this review is to describe new advances in our knowledge regarding the role of MTHFR, KCNK18, TRPV1, TRPV3 and HCRTR genes in primary headache disorders. Involvement of these genes in primary headaches, as well as their potential role in the therapy of these disorders, will be discussed

Orexin Receptor Multimerization versus Functional Interactions: Neuropharmacological Implications for Opioid and Cannabinoid Signalling and Pharmacogenetics

Peer reviewe

Decreased resistin plasmatic concentrations in patients with Alzheimer's disease: A case-control study

Previous studies suggested a role for adipokines in ageing and in several age-related diseases. The purpose of our study was to further elucidate adipokines involvement in neurodegeneration, investigating adiponectin, leptin and resistin in Alzheimer's disease (AD) and Frontotemporal Dementia (FTD). We enrolled for the study 70 subjects: 26 AD, 21 FTD, and 23 with other neurological (but not neurodegenerative) conditions (CTR, control group). According to a standardized protocol, we measured adipokines plasmatic levels, blood parameters of glucidic and lipidic metabolism, ESR, cerebrospinal fluid (CSF) markers of neurodegeneration (beta-amyloid, total-Tau, phosphorylated-Tau) and anthropometric parameters. In comparison with control group, we found lower resistin concentrations in patients with dementia, and in particular in AD (p < 0.001). In multivariate analysis, AD relative risk was reduced by resistin, when controlling for sex, age and anthropometric/metabolic parameters (RR = 0.71, P < 0.0001). Considering CSF biomarkers, we found a direct correlation between resistin and Aβ(1-42) CSF concentration in patients (p < 0.001, r = 0.50). Lower resistin characterized AD patients in our study and AD, but not FTD, diagnosis risk was found to be inversely associated with resistin when controlling for confounders. We hypothesize that resistin-linked metabolic profile has to be reconsidered and further investigated in AD