Martinez-Valbuena, I. (Iván)
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- Excess abdominal fat is associated with cutaneous allodynia in individuals with migraine: a prospective cohort study(2020) Irimia, P. (Pablo); Frühbeck, G. (Gema); Mínguez-Olaondo, A. (Ane); Martinez-Valbuena, I. (Iván); Martinez-Vila, E. (Eduardo); Romero, S. (Sonia); Luquin, M.R. (María Rosario)Objective: To investigate the specific relationship between cutaneous allodynia (CA) and the percentages of body fat (BF) and abdominal fat in migraineurs. Additionally, we compared serum levels of inflammatory biomarkers in patients with and without CA. Background: Excess abdominal fat might facilitate progressive changes in nociceptive thresholds causing central sensitization, clinically reflected as CA, which could drive migraine progression. Methods: This prospective cohort study included 80 patients with migraine (mean age 39 years, 81.2% female) and 39 non-migraine controls. We analysed each participant’s height, body weight, and body mass index (BMI). The amount and distribution of BF was also assessed by air displacement plethysmography (ADP) and ViScan, respectively. We analysed serum levels of markers of inflammation, during interictal periods. Results: We studied 52 patients with episodic migraine (EM) and 28 with chronic migraine (CM). Of the 80 patients, 53 (53.8%) had CA. Migraineurs with CA had a higher proportion of abdominal fat values than patients without CA (p = 0.04). The independent risk factors for CA were the use of migraine prophylaxis (OR 3.26, 95% CI [1.14 to 9.32]; p = 0.03), proportion of abdominal fat (OR 1.13, 95% CI [1.01 to 1.27]; p = 0.04), and presence of sleep disorders (OR 1.13, 95% CI [00.01 to 1.27]; p = 0.04). The concordance correlation coefficient between the ADP and BMI measurements was 0.51 (0.3681 to 0.6247). CA was not correlated with the mean plasma levels of inflammatory biomarkers. Conclusions: There is a relation between excess abdominal fat and CA. Abdominal obesity might contribute to the development of central sensitization in migraineurs, leading to migraine chronification.
- CAV-2-Mediated GFP and LRRK2G2019S Expression in the Macaca fascicularis Brain(2020) Gennetier, A. (Aurelie); Carmona-Abellán, M.M. (María del Mar); Kremer, E.J. (Eric J.); Marcilla-Garcia, I. (Irene); Martinez-Valbuena, I. (Iván); Carril-Mundiñano, I. (Iñaki); Luquin, M.R. (María Rosario); Hernandez, M. (María); Di-Caudo, C. (Carla)Parkinson’s disease is characterized by motor and nonmotor symptoms that gradually appear as a consequence of the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Currently, no treatment can slow Parkinson’s disease progression. Inasmuch, there is a need to develop animal models that can be used to understand the pathophysiological mechanisms underlying dopaminergic neuron death. The initial goal of this study was to determine if canine adenovirus type 2 (CAV-2) vectors are effective gene transfer tools in the monkey brain. A second objective was to explore the possibility of developing a large nonhuman primate that expresses one of the most common genetic mutations causing Parkinson’s disease. Our studies demonstrate the neuronal tropism, retrograde transport, biodistribution, and efficacy of CAV-2 vectors expressing GFP and leucine-rich repeat kinase 2 (LRRK2G2019S) in the Macaca fascicularis brain. Our data also suggest that following optimization CAV-2-mediated LRRK2G2019S expression could help us model the neurodegenerative processes of this genetic subtype of Parkinson’s disease in monkeys.
- JNK Activation in Alzheimer's Disease Is Driven by Amyloid β and Is Associated with Tau Pathology(2023) Vela, S. (S.); Ramirez, M.J. (María Javier); Smerdou, C. (Cristian); Solas, M. (Maite); Martisova, E. (Eva); Martinez-Valbuena, I. (Iván); Luquin, M.R. (María Rosario)c-Jun N-terminal kinase 3 (JNK3) is suggested to play a key role in neurodegenerative disorders, especially in Alzheimer's disease (AD). However, it remains unclear whether JNK or amyloid β (Aβ) appears first in the disease onset. Postmortem brain tissues from four dementia subtypes of patients (frontotemporal dementia, Lewy body dementia, vascular dementia, and AD) were used to measure activated JNK (pJNK) and Aβ levels. pJNK expression is significantly increased in AD; however, similar pJNK expression was found in other dementias. Furthermore, there was a significant correlation, co-localization, and direct interaction between pJNK expression and Aβ levels in AD. Significant increased levels of pJNK were also found in Tg2576 mice, a model of AD. In this line, Aβ42 intracerebroventricular injection in wild-type mice was able to induce a significant elevation of pJNK levels. JNK3 overexpression, achieved by intrahippocampal injection of an adeno-associated viral vector expressing this protein, was enough to induce cognitive deficiencies and precipitate Tau aberrant misfolding in Tg2576 mice without accelerating amyloid pathology. JNK3 overexpression may therefore be triggered by increased Aβ. The latter, together with subsequent involvement of Tau pathology, may be underlying cognitive alterations in early stages of AD.
- JNK3 overexpression in the entorhinal cortex impacts on the hippocampus and induces cognitive deficiencies and Tau misfolding(2023) Bejarano, A. (A.); Ezkurdia-Lasarte, A. (Amaia); Echarte, B. (B.); Smerdou, C. (Cristian); Solas, M. (Maite); Ramírez-Gil, M. (María); Martisova, E. (Eva); Martinez-Valbuena, I. (Iván); García-Ardanaz, C. (Carlos); Luquin-Piudo, M.R. (María Rosario)c-Jun N-terminal kinases (JNKs) are a family of proteinkinasesactivated by a myriad of stimuli consequently modulating a vast rangeof biological processes. In human postmortem brain samples affectedwith Alzheimer ' s disease (AD), JNK overactivation has beendescribed; however, its role in AD onset and progression is stillunder debate. One of the earliest affected areas in the pathologyis the entorhinal cortex (EC). Noteworthy, the deterioration of theprojection from EC to hippocampus (Hp) point toward the idea thatthe connection between EC and Hp is lost in AD. Thus, the main objectiveof the present work is to address if JNK3 overexpression in the ECcould impact on the hippocampus, inducing cognitive deficits. Dataobtained in the present work suggest that JNK3 overexpression in theEC influences the Hp leading to cognitive impairment. Moreover, proinflammatorycytokine expression and Tau immunoreactivity were increased both inthe EC and in the Hp. Therefore, activation of inflammatory signalingand induction of Tau aberrant misfolding caused by JNK3 could be responsiblefor the observed cognitive impairment. Altogether, JNK3 overexpressionin the EC may impact on the Hp inducing cognitive dysfunction andunderlie the alterations observed in AD.
- Behavioral duality in an integrated agent(Frontiers, 2014) Bernácer-María, J. (Javier); Martinez-Valbuena, I. (Iván)