Prevalencia de patología dual en el sur del Perú: estudio clínico-descriptivo

Comorbidity between substance use disorders and other psychiatric disorders or dual diagnosis (PD) is characterized by difficulty in their therapeutic approach, constant relapses and hospital admissions, as well as higher violent and criminal behavior. Our objective was to determine the prevalence of PD in individuals treated at a psychiatric center in Arequipa, Peru. It is a descriptive epidemiological study based on analysis of 445 case histories (HC) of patients admitted during the period of three years (2011-2013). Socio-demographic and clinical characteristics of subjects by comparing those who had a diagnosis of PD, with those who had a diagnosis just by consuming psychotropic substances were established. The results show a prevalence of dual diagnosis in 49%. The average ages were M = 31.45, DS = 15.59 in the with dual diagnosis group CPD and M = 33.93, DS = 15.48 in the without dual diagnosis group SPD; the prevalence of substance use was 51% SPD. Alcohol was the most used substance, followed by cannabis marijuana and cocaine base (PBC). The socio-family and individual vulnerability of the population is evidence for protection or resistance to mental illness, as well as the lack of implementation of effective policies in mental health care for dual disorders, showing worse prognosis and indexes every time higher.La comorbilidad entre un trastorno por uso de sustancias y otros trastornos psiquiátricos o patología dual (PD) se caracteriza por la dificultad en su abordaje terapéutico, recaídas constantes e ingresos hospitalarios. Nuestro objetivo fue conocer la prevalencia de PD en un centro psiquiátrico de Arequipa-Perú. Es un estudio descriptivo epidemiológico basado en el análisis de 445 historias clínicas (HC) de pacientes ingresados durante el lapso de tres años (periodo 2011-2013). Se establecieron características sociodemográficas y clínicas de los sujetos comparando entre quienes presentaron un diagnóstico de PD, con aquellos que solo tuvieron diagnóstico por consumo de sustancias psicótropas. Los resultados evidencian una prevalencia de patología dual de 49%. Las edades promedio fueron de M = 31.45, DE = 15.59 en el grupo con patología dual (CPD) y M = 33.93, DE = 15.48 en el grupo sin patología dual (SPD); la prevalencia del consumo de sustancias SPD fue del 51%. El alcohol fue la sustancia más consumida, seguida de cannabis, marihuana y la pasta básica de cocaína (PBC). Se evidencia la vulnerabilidad socio-familiar e individual de la población en cuanto a protección o resistencia frente a la enfermedad mental, además de la carencia de políticas efectivas en salud mental, que muestran peor pronóstico e índices cada vez más elevados

Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of MiceWas Reduced in Aging.

Aging is accompanied by a decline in cognition that can be due to a lower IGF-I level. We studied response facilitation induced in primary somatosensory (S1) cortical neurons by repetitive stimulation of whiskers in young and old mice. Layer 2/3 and 5/6 neurons were extracellularly recorded in young ( 6 months of age) and old ( 20 month of age) anesthetized mice. IGF-I injection in S1 cortex (10 nM; 0.2 L) increased whisker responses in young and old animals. A stimulation train at 8 Hz induced a long-lasting response facilitation in only layer 2/3 neurons of young animals. However, all cortical neurons from young and old animals showed long-lasting response facilitation when IGF-I was applied in the S1 cortex. The reduction in response facilitation in old animals can be due to a reduction in the IGF-I receptors as was indicated by the immunohistochemistry study. Furthermore, a reduction in the performance of a whisker discrimination task was observed in old animals. In conclusion, our findings indicate that there is a reduction in the synaptic plasticity of S1 neurons during aging that can be recovered by IGF-I. Therefore, it opens the possibility of use IGF-I as a therapeutic tool to ameliorate the effects of heathy aging.post-print2685 K

Astrocytic IGF-IRs induce adenosine-mediated inhibitory downregulation and improve sensory discrimination

Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory processes. While the effects of IGF-I on neurons have been studied extensively, the involvement of astrocytes in IGF-I signaling and the consequences on synaptic plasticity and animal behavior remain unknown. We have found that IGF-I induces long-term potentiation (LTPIGFI) of the postsynaptic potentials that is caused by a long-term depression of inhibitory synaptic transmission in mice. We have demonstrated that this long-lasting decrease in the inhibitory synaptic transmission is evoked by astrocytic activation through its IGF-I receptors (IGF-IRs). We show that LTPIGFI not only increases the output of pyramidal neurons, but also favors the NMDAR-dependent LTP, resulting in the crucial information processing at the barrel cortex since specific deletion of IGF-IR in cortical astrocytes impairs the whisker discrimination task. Our work reveals a novel mechanism and functional consequences of IGF-I signaling on cortical inhibitory synaptic plasticity and animal behavior, revealing that astrocytes are key elements in these processesThis work was supported by Grants BFU2016-80802-P from Agencia Estatal de Investigación Spain/Fondo Europeo de Desarrollo Regional, and from the European Union [Ministerio de Economía y Competitividad (MINECO)] to D.F.d.S.; Grants R01-NS-097312 and R01-DA-048822 from National Institutes of Health/National Institute of Neurological Disorders and Stroke to A.A.; and grants from Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) and Grant SAF2016-76462-C2-1-P from MINECO to I.T.-A. J.A.Z.-V. was supported by the National Council of Science, Technology and Technological Innovation (CONCYTEC, Perú) through the National Fund for Scientific and Technological Development (FONDECYT, Perú). J.F. received a postdoctoral fellowship from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; Grants #2017/ 14742-0 and #2019/03368-5). We thank the University of Minnesota Viral Vector and Cloning Core for production of some of the viral vectors used in this study; and Dr. G. Perea and Dr. Washington Buño for helpful comment

Prevalencia de patología dual en el sur del Perú: estudio clínico-descriptivo

La comorbilidad entre un trastorno por uso de sustancias y otros trastornos psiquiátricos o patología dual (PD) se caracteriza por la dificultad en su abordaje terapéutico, recaídas constantes e ingresos hospitalarios. Nuestro objetivo fue conocer la prevalencia de PD en un centro psiquiátrico de Arequipa-Perú. Es un estudio descriptivo epidemiológico basado en el análisis de 445 historias clínicas (HC) de pacientes ingresados durante el lapso de tres años (periodo 2011-2013). Se establecieron características sociodemográficas y clínicas de los sujetos comparando entre quienes presentaron un diagnóstico de PD, con aquellos que solo tuvieron diagnóstico por consumo de sustancias psicótropas. Los resultados evidencian una prevalencia de patología dual de 49%. Las edades promedio fueron de M = 31.45, DE = 15.59 en el grupo con patología dual (CPD) y M = 33.93, DE = 15.48 en el grupo sin patología dual (SPD); la prevalencia del consumo de sustancias SPD fue del 51%. El alcohol fue la sustancia más consumida, seguida de cannabis, marihuana y la pasta básica de cocaína (PBC). Se evidencia la vulnerabilidad socio-familiar e individual de la población en cuanto a protección o resistencia frente a la enfermedad mental, además de la carencia de políticas efectivas en salud mental, que muestran peor pronóstico e índices cada vez más elevados

The Role of Insulin-like Growth Factor I in Mechanisms of Resilience and Vulnerability to Sporadic Alzheimer’s Disease

Despite decades of intense research, disease-modifying therapeutic approaches for Alzheimer’s disease (AD) are still very much needed. Apart from the extensively analyzed tau and amyloid pathological cascades, two promising avenues of research that may eventually identify new druggable targets for AD are based on a better understanding of the mechanisms of resilience and vulnerability to this condition. We argue that insulin-like growth factor I (IGF-I) activity in the brain provides a common substrate for the mechanisms of resilience and vulnerability to AD. We postulate that preserved brain IGF-I activity contributes to resilience to AD pathology as this growth factor intervenes in all the major pathological cascades considered to be involved in AD, including metabolic impairment, altered proteostasis, and inflammation, to name the three that are considered to be the most important ones. Conversely, disturbed IGF-I activity is found in many AD risk factors, such as old age, type 2 diabetes, imbalanced diet, sedentary life, sociality, stroke, stress, and low education, whereas the Apolipoprotein (Apo) E4 genotype and traumatic brain injury may also be influenced by brain IGF-I activity. Accordingly, IGF-I activity should be taken into consideration when analyzing these processes, while its preservation will predictably help prevent the progress of AD pathology. Thus, we need to define IGF-I activity in all these conditions and develop a means to preserve it. However, defining brain IGF-I activity cannot be solely based on humoral or tissue levels of this neurotrophic factor, and new functionally based assessments need to be developed.This research was funded by the Spanish Ministry of Science (PID2019-104376RB-I00 (AEI/FEDER, UE)

The neurobiology of insulin-like growth factor I: From neuroprotection to modulation of brain states

After decades of research in the neurobiology of IGF-I, its role as a prototypical neurotrophic factor is undisputed. However, many of its actions in the adult brain indicate that this growth factor is not only involved in brain development or in the response to injury. Following a three-layer assessment of its role in the central nervous system, we consider that at the cellular level, IGF-I is indeed a bona fide neurotrophic factor, modulating along ontogeny the generation and function of all the major types of brain cells, contributing to sculpt brain architecture and adaptive responses to damage. At the circuit level, IGF-I modulates neuronal excitability and synaptic plasticity at multiple sites, whereas at the system level, IGF-I intervenes in energy allocation, proteostasis, circadian cycles, mood, and cognition. Local and peripheral sources of brain IGF-I input contribute to a spatially restricted, compartmentalized, and timed modulation of brain activity. To better define these variety of actions, we consider IGF-I a modulator of brain states. This definition aims to reconcile all aspects of IGF-I neurobiology, and may provide a new conceptual framework in the design of future research on the actions of this multitasking neuromodulator in the brain.We thank past members of the lab for their contributions and long-term funding support from Ciberned and the Spanish Ministerio de Ciencia e Innovación