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La Agencia Estatal Consejo Superior de Investigaciones Científicas (CSIC) es la mayor institución pública dedicada a la investigación en España y la tercera de Europa. Adscrita al Ministerio de Economía y Competitividad, a través de la Secretaría de Estado de Investigación, Desarrollo e Innovación, su objetivo fundamental es desarrollar y promover investigaciones en beneficio del progreso científico y tecnológico, para lo cual está abierta a la colaboración con entidades españolas y extranjeras. El CSIC desempeña un papel central en la política científica y tecnológica, ya que abarca desde la investigación básica a la transferencia del conocimiento al sector productivo. El motor de la investigación lo forman sus centros e institutos, distribuidos por todas las comunidades autónomas, y sus más de 15.000 trabajadores, de los cuales más de 3.000 son investigadores en plantilla y otros tantos doctores y científicos en formación. El CSIC cuenta con el 6 por ciento del personal dedicado a la Investigación y el Desarrollo en España, que genera aproximadamente el 20 por ciento de la producción científica nacional. Además, gestiona un conjunto de importantes infraestructuras, la red más completa y extensa de bibliotecas especializadas y cuenta con unidades mixtas de investigación. http://www.csic.es/

Entrevista con la Dra. Coral Sanfeliu

Fuente: Excodra | Publicado: 08-09-2017
Todo el cuerpo envejece y el cerebro no es una excepción. En ausencia de enfermedades neurodegenerativas el deterioro cerebral en el envejecimiento es leve. Las neuronas no mueren con la edad. Aunque eso sí, algunas encogen de tamaño. Esta atrofia se ha detectado en las neuronas piramidales de la corteza cerebral y del hipocampo, dos regiones muy importantes para los mecanismos de memoria.
Derechos: Dra. Coral Sanfeliu
28 comentarios

Coral, para comenzar, ¿qué características tiene el envejecimiento cerebral, en qué consiste principalmente y, tiene rasgos particulares que lo diferencien del envejecimiento del resto de órganos?

Todo el cuerpo envejece y el cerebro no es una excepción. En ausencia de enfermedades neurodegenerativas el deterioro cerebral en el envejecimiento es leve. Las neuronas no mueren con la edad. Aunque eso sí, algunas encogen de tamaño. Esta atrofia se ha detectado en las neuronas piramidales de la corteza cerebral y del hipocampo, dos regiones muy importantes para los mecanismos de memoria. También hay una disminución de las conexiones. En el cerebro adulto se estima que hay al menos 1014 conexiones sinápticas entre unas 1011 neuronas y en regiones sensibles se pueden perder hasta un 0,5 % de conexiones por año entre las edades de juventud y vejez. En consecuencia va a disminuir un poco la capacidad de transmitir información entre las neuronas. Los efectos más frecuentes son sobre velocidad de razonamiento y percepción visual. En cuanto a la memoria se deteriora principalmente la memoria episódica, es decir la capacidad de contextualizar nuestros recuerdos. En conjunto, nada grave por suerte.



Las causas moleculares del envejecimiento creemos que son comunes a todos los tejidos. Desde las teorías iniciales se ha evolucionado a situar el estrés celular derivado de la propia actividad como causante de una desestabilización de los diversos procesos celulares.


Otro componente son los cambios en la expresión de genes, como comentaba Carlos Dotti en este mismo foro. Antes de la pérdida funcional irreversible tenemos el periodo de fragilidad, con pérdida de la capacidad de respuesta a los estímulos nocivos para recuperar este equilibrio celular. En nuestra investigación del envejecimiento cerebral nos interesa definir mecanismos de resiliencia como defensa contra el establecimiento de la fragilidad. Los cambios moleculares del envejecimiento son factores de riesgo para una serie de enfermedades, por tanto una mayor resiliencia cerebral también protegerá contra las enfermedades neurodegenerativas.

Acabáis de publicar “Proinsulin protects against age-related cognitive loss through anti-inflammatory convergent pathways” en la revista Neuropharmacology, con varios grupos de investigación implicados. Por un lado, ¿cómo funciona exactamente la proinsulina como neuroprotector, qué la convierte en un neurofárrmaco tan atractivo? Y por otro, ¿cómo se desenvolvió la participación de los grupos implicados en el estudio para llevar el trabajo a término?

Sí, en efecto, en un trabajo conjunto entre Enrique de la Rosa experto en proinsulina, Fátima Bosch que diseñó los vectores virales para el tratamiento y nosotros, hemos demostrado que la proinsulina protege de la pérdida de memoria en ratones de una cepa de senescencia acelerada (SAMP8). El estudio del tejido del hipocampo nos permitió detectar que la proinsulina induce la activación de una vía molecular de supervivencia y neuroprotección (PI3/Akt) y como efecto final disminuye la inflamación cerebral. Procesamos todos los datos por teoría de grafos que indicó que la reactividad crónica de los astrocitos era el evento central en la red de cambios inducidos por proinsulina. Neuroinflamación importante y pérdida de memoria son ejes básicos en el envejecimiento patológico, en la zona ya cercana a los cambios irreversibles hacia la demencia. Por tanto creemos que la proinsulina tiene potencial como fármaco antienvejecimiento cerebral.

Pero déjame volver un poco atrás porque la gestación de este estudio –como todos– ha sido apasionante. La proinsulina es el precursor de la insulina pero por estudios previos en el laboratorio de Enrique de la Rosa sabíamos que podía ser un factor que activara por sí solo mecanismos de supervivencia, como un miembro más de la familia de insulina y factores de crecimiento insulínico. Nuestro objetivo inicial era proteger la retina en ratones senescentes. Fue fantástico descubrir los beneficios cognitivos de la proinsulina.

Este estudio se desarrolló dentro de un proyecto Consolider (BrainAge, coordinado por C. Dotti), un programa excelente de financiación de proyectos científicos en consorcio que permitió –en las pocas ediciones que hubo– el sinergismo entre grupos de investigación españoles. A pesar de las movilizaciones de numerosos investigadores, no hemos conseguido su reedición. Es decepcionante la poca inversión en I+D año tras año, con crisis o sin ella, que sigue estando lejos de la media europea.

En vuestro grupo trabajáis con el neuroprotector Resveratrol, ¿cómo es esta molécula, en qué eventos participa para tener relevancia en el tratamiento/prevención del Alzheimer?

El resveratrol es una molécula que fabrican muchas plantas para activar mecanismos de defensa contra el estrés y las lesiones. Se encuentra en buena concentración en uvas, frutos rojos, cacahuetes y cacao. Se atribuyen principalmente al resveratrol los efectos beneficiosos del consumo moderado de vino tinto. Tiene un gran poder antioxidante entre otras acciones, pero lo que nos interesa en nuestro laboratorio es su capacidad de activar las sirtuínas, moléculas en las que llevamos tiempo trabajando. Las sirtuínas son enzimas claves en vías moleculares de supervivencia celular.



En modelos de ratón de la enfermedad de Alzheimer hemos demostrado recientemente que la sobre expresión génica de sirtuína 1 en el hipocampo aumenta los mecanismos cerebrales de destrucción y limpieza de proteínas aberrantes en las neuronas y restaura la capacidad de aprendizaje y la memoria.


Ahora estamos finalizando un estudio similar con la administración de resveratrol como suplemento en la comida de estos ratones enfermos, en el que se ha reproducido una recuperación total. No sólo eso sino que también se activan mecanismos moleculares de mejora de memoria en los ratones sanos del grupo control que recibían resveratrol. Es decir, que podemos decir que el resveratrol aumenta la resiliencia cerebral contra posibles futuras patologías.

El paso a la clínica del resveratrol en la enfermedad de Alzheimer presenta dificultades todavía por resolver en cuanto a una formulación química que mejore la biodisponibilidad. Los estudios clínicos son escasos, aunque en uno de ellos se han detectado cambios positivos en pacientes en fases poco avanzadas de la enfermedad. Sí se han visto claras mejoras cognitivas con resveratrol en voluntarios sanos de edad avanzada, lo que estaría de acuerdo con nuestros hallazgos de incremento de mecanismos promotores de resiliencia.

Investigáis también con los astrocitos, cuéntanos por favor sobre este tipo de células, de las que cada vez se está viendo cuán relevantes son en la estructura funcional del cerebro, qué participación tienen en los procesos de envejecimiento, de protección contra la degeneración neuronal.

Los astrocitos están en nuestro cerebro no sólo acompañando sino también trabajando codo a codo con las neuronas. Inicialmente, se les atribuyó un papel pasivo de proveedores de soporte físico y de nutrientes a las neuronas. Cajal ya puso en duda este papel tan secundario, siguiendo su genialidad en la interpretación funcional de las células del sistema nervioso. Ha pasado un siglo y las técnicas moleculares de las últimas décadas han permitido demostrar que los astrocitos son excitables mediante corrientes de calcio intracelular y se comunican también con mediadores químicos entre ellos y con las neuronas. Para ello se integran con las redes neuronales y modulan la transmisión de la información entre dos neuronas mediante las conexiones de sinapsis tripartita (dos neuronas y un astrocito) que han caracterizado Alfonso Araque y Gertrudis Perea.

Nos interesa estudiar el papel de los astrocitos en situaciones de deterioro cognitivo y senescencia. Efectivamente, en una serie de trabajos in vitro vimos que los astrocitos senescentes disminuían su capacidad neuroprotectora y sufrían cambios que contribuyen en gran medida al estrés oxidativo y la neuroinflamación en el cerebro envejecido y frágil. Como terapia in vivo ensayamos la sobre expresión de un factor trófico propio de los astrocitos, el GDNF, en los astrocitos de hipocampo de ratas viejas deficientes y de ratones transgénicos de Alzheimer. En ambos casos se produjo una total recuperación de la memoria y del estado celular cerebral.



Los astrocitos tienen mayor resistencia al estrés y las lesiones que las neuronas y a su vez son neuroprotectores. Si damos con los mecanismos adecuados para su estimulación podrían ser una diana para promover resiliencia cerebral frente a las enfermedades neurodegenerativas.


Extrapolar los resultados obtenidos en modelos murinos a lo que ocurre en humanos no siempre es fácil, ¿cómo trabajáis la parte de vuestros estudios centrada en terapias contra la neurodegeneración? ¿Qué características tienen vuestros ratones transgénicos para poder relacionarlos con los sucesos biológicos en humanos, en cuanto a terapias preventivas?

Los animales de laboratorio hacen un gran servicio a la sociedad en el estudio de enfermedades, desarrollo de terapias, vacunas, etc. Quiero insistir en el absoluto control que hay en usar los mínimos posibles y evitarles cualquier sufrimiento. En nuestro laboratorio también usamos cultivos celulares para estudiar algunos mecanismos moleculares y sangre de voluntarios sanos y de pacientes para algunas caracterizaciones, pero no podemos renunciar de momento al uso de modelos murinos.

En el envejecimiento cerebral normal, para estudiar pérdidas leves de memoria hemos usado ratas y ratones de edad avanzada que en estas especies es a los 20-24 meses. Los humanos compartimos alrededor del 99% de genes con estos animales. Son un modelo animal válido para mecanismos conservados en la evolución, pero siempre habrá incertezas. El ratón SAMP8 de senescencia acelerada, obtenido por selección fenotípica, ya presenta mayor pérdida cognitiva y rasgos de envejecimiento patológico. Útil para estudiar la prevención de la neurodegeneración.

Sin duda, los animales de laboratorio más utilizados en la investigación del Alzheimer son los ratones transgénicos. Hemos usado cepas con múltiples transgenes que inducen un fenotipo agresivo (5XFAD y 3xTg-AD). En general reproducen el curso progresivo de los cambios patológicos cerebrales y de pérdida de aprendizaje y memoria y también cambios en el espectro no cognitivo, como ansiedad, apatía, etc. Sin embargo, la mayoría de los casos de la población son no hereditarios, sin causa conocida, y el curso de la enfermedad es mucho más lento y complicado que en el Alzheimer familiar, y ya tenemos aquí un salto difícil para extrapolar. Ahora se están desarrollando los modelos de Alzheimer de segunda generación en que sus neuronas expresan secuencias humanizadas con las mutaciones del Alzheimer familiar en el gen propio del ratón. Estos ratones generan amiloide pero sin pérdida de memoria u otros cambios significativos. Podrían ser un modelo de la larga fase preclínica silente que hay en la enfermedad, que puede alargarse se cree unos 20 años. Tenemos modelos parciales de la enfermedad, por tanto la extrapolación de una terapia protectora se referirá siempre a una protección parcial que puede ser más o menos relevante. La última palabra es de los estudios clínicos.

Resumiendo un poco lo anterior, la pérdida de facultades cognitivas, con el paso de los años, con el envejecimiento, es un hecho, claro, sin tener que estar ligado a enfermedades como el Alzheimer, por ejemplo. Entonces, trabajando la prevención, con fármacos neuroprotectores, con dietas determinadas y ejercicio físico controlado, ¿hasta dónde podría llegar el ser humano, y cómo, si consigue un buen equilibrio desde la prevención del envejecimiento? ¿Qué se espera de estos avances en los próximos años?

La prevención es importantísima y nos afecta a todos a todas las edades. Cuidando la salud y el estilo de vida veremos aumentar el número de centenarios con todas sus facultades mentales. El límite de longevidad no lo conocemos, pero se ha sugerido que podremos llegar con salud a los 125 años. Yendo más lejos, existe una corriente de investigadores que dicen que en pocas décadas todas las enfermedades que aparecen en la vejez se podrán curar y ya no vamos a morir. Además le han puesto fecha, el año 2045. La idea es dar con un fármaco anti-envejecimiento que va a rejuvenecer todos los tejidos. Y cuando falle un órgano podrá reemplazarse por uno fabricado, seremos avatares dicen. Sin llegar a este extremo, sí que en pocos años puede haber fármacos que protejan de diversos aspectos del desequilibrio y pérdida de funciones celulares. Justo se ha despertado el interés de las compañías farmacéuticas por el envejecimiento y en este 2017 está en marcha un estudio clínico de longevidad con metformina que es un antidiabético, para comprobar si en humanos protege contra inflamación, daño oxidativo, disminución del procesamiento de proteínas aberrantes y otros aspectos de la senescencia celular y con ello previene enfermedades de la vejez.



En el informe de la Comisión Lancet sobre demencia (publicado en The Lancet en Julio 2017), se insistía en que la única forma por el momento de parar lo que podría ser una epidemia de demencia es adquirir o cambiar una serie de hábitos de estilos de vida y controlar las enfermedades crónicas.


Estas recomendaciones tienen estudios clínicos detrás que demuestran que disminuyen el riesgo de sufrir Alzheimer, y muchísimos estudios básicos sobre los mecanismos neuroprotectores. La dieta mediterránea o similarmente rica en antioxidantes y nutrientes y ejercicio físico regular son neuroprotectores. Además hace años que se conoce que una buena educación y mantener la actividad intelectual toda la vida proporciona reserva cognitiva que sube el listón del grado de patología cerebral necesario para caer en la demencia. Mejorar los problemas de obesidad, hipertensión, inflamación, diabetes, etc., redundará en beneficios cerebrales. Por supuesto hay que añadir que el estrés excesivo, poca calidad de sueño, fumar y otros hábitos tóxicos es nocivo, mientras que tener amigos y hacer actividades sociales es bueno para nuestro cerebro.

En nuestra investigación, hemos analizado los mecanismos neuroprotectores y activadores de resiliencia cerebral de ejercicio físico y suplementos dietarios. Vemos activación de la vía de las sirtuínas que comentaba antes, y mecanismos neurotróficos y antiinflamatorios. Sobre el ejercicio estamos acabando un proyecto de marcadores de resiliencia en sangre de voluntarios de edad madura con largo historial de actividad física, se trata de jugadores de rugby, ha sido muy gratificante su colaboración. Quiero pensar que contribuimos a cambiar el abordaje que se da en la sociedad a la importancia de la prevención.

En fin, con vida saludable y con la ayuda adicional de fármacos o sin ellos, creo que sí veremos grandes cambios en nuestros ancianos, mayor longevidad y envejecimiento con salud plena hasta los últimos años y menor incidencia de enfermedades de la vejez.

Más en concreto, sobre el Alzheimer, ¿cuánto camino nos queda por recorrer para tratarlo una vez que aparece? ¿Cuáles son las principales vías de investigación que están teniendo más éxito?

Nos queda mucho camino, pero se van cerrando etapas. Hasta ahora sólo hemos curado ratones porque los resultados de la inmensa mayoría de los ensayos clínicos con pacientes de Alzheimer han sido negativos, es terriblemente decepcionante. Para un enfermo diagnosticado sólo hay tratamiento sintomático con unos pocos fármacos aprobados (inhibidores de colinesterasa y un antagonista de NMDA). Eso sí, es muy importante todo el soporte social y familiar y una vida activa mientras sea posible para enlentecer al máximo la progresión. Las asociaciones están haciendo una labor importantísima.



Actualmente entre los resultados clínicos más prometedores tenemos la inmunoterapia contra el amiloide. Una segunda generación de anticuerpos más específica y con menos efectos secundarios, comienza a ser efectiva. Los efectos cognitivos son todavía discretos debido a la gran carga amiloidea en los pacientes. La tendencia es trasladar los ensayos clínicos a fases iniciales de la patología.


Interesaría iniciar los tratamientos incluso a la fase preclínica, para ello se está trabajando en biomarcadores en sangre que faciliten la detección precoz. Es posible que en estas fases sí se vean efectos de algunos fármacos que han sido neuroprotectores en los modelos transgénicos. En nuestro laboratorio, además de seguir las investigaciones en vías moleculares de neuroprotección, estamos estudiando activar la proteolisis celular de proteínas aberrantes.

Hay una presión global para acabar con el Alzheimer en este siglo XXI. Confío en que lograremos bajar las cifras espeluznantes de 47 millones de personas con demencia en 2015, de las que aproximadamente el 60% son casos de Alzheimer. Pero se necesitará más inversión y el esfuerzo de todos. Si no, con el aumento de la esperanza de vida, se calcula que habría el triple de casos en 2050.
 
Para terminar, Coral, los estudios en Neurociencias son apasionantes, y saliéndonos un poco del tema, pero no mucho, la conservación de la conciencia de nosotros mismos y de la memoria, durante el envejecimiento es capital para mantenernos como personas íntegras. Entonces, ¿qué están aportando, precisamente, los estudios en neurodegeneración al entendimiento de lo que sea la conciencia y sus bases biológicas?

Hemos avanzado mucho en el conocimiento del cerebro, la estructura de las redes neuronales y gliales y su funcionamiento. Conocemos parte de los mecanismos moleculares de la memoria que nos permiten almacenar y luego recuperar recuerdos del pasado y con ellos saber quién somos. Pero no conocemos las bases biológicas de la conciencia de uno mismo que incluiría el reconocimiento del yo individual, de nuestras emociones y de nuestra relación con otros individuos. La relación entre cerebro y conciencia es uno de los grandes misterios de la ciencia pendientes de resolver como dice Rick Hanson, neuropsicólogo y divulgador de los beneficios de la meditación. Sí hay consenso en que la actividad cerebral es el sustrato de la mente y, entre los fenómenos mentales generados, la conciencia sería consecuencia de las actividades cerebrales más complejas de áreas superiores corticales. No hay certeza sobre si los individuos de otras especies también tienen un cierto grado de alerta consciente.

El deterioro de las actividades cerebrales del Alzheimer lleva obviamente a la pérdida de conciencia de uno mismo como individuo, pero no en las fases iniciales en que los enfermos son conscientes de que tienen un problema, de que pierden memoria y necesitan ayuda. Esta pérdida de conciencia también pasa en otras enfermedades con extensas lesiones, pero no en el envejecimiento. Incluso yo diría que con la edad y las vivencias acumuladas aumenta la sensación de identidad de los abuelos entrañables, aunque no hay estudios.

De nuevo se puede hacer prevención ejercitando la mente. Las técnicas de ejercitar la memoria y funciones ejecutivas son válidas, pero también las técnicas de meditación tienen sus beneficios. Se han demostrado cambios funcionales y estructurales en el cerebro de meditadores expertos. Las técnicas de meditación, especialmente la intervención de “atención plena” (mindfulness) que aumenta el estado mental de conciencia, se están probando en enfermos de Alzheimer como terapia añadida a los fármacos o en cortas intervenciones y los resultados apoyan sus beneficios. Cultivar la conciencia de que tenemos conciencia es fascinante como transformadora de nuestro cerebro, nos queda muchísimo por aprender.


Enlace a grupo de investigación: https://www.iibb.csic.es/es/research/53
Comentarios:
 
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Coral Sanfeliu

Coral Sanfeliu

Es investigadora del Instituto de Investigaciones Biomédicas de Barcelona (IIBB), CSIC, y del Institut d’Investigacions Biomédiques August Pi i Sunyer (IDIBAPS). Doctora en Biología por la Universidad Autónoma de Barcelona (1985). Realizó estancias en el National Institute for Medical Research, MRC, Londres, UK (1988-1989) y en la University of British Colombia, Vancouver, Canadá (1995-1996). Desde 2003 dirige el grupo de investigación de Envejecimiento y Neurodegeneración en el IIBB, creado en respuesta al reto de proteger contra la pérdida cognitiva y el riesgo de Alzhéimer en el envejecimiento cerebral. La investigación básica en modelos animales y cultivos celulares se completa con un enfoque translacional mediante colaboraciones con grupos clínicos. Desde la fundación del grupo, Sanfeliu ha dirigido 10 proyectos de investigación (FIS, MEC y fundaciones) y ha participado en redes cooperativas nacionales e internacionales (RETICEF, CIBER BrainAge, COST MouseAge). Los principales logros publicados se centran en la activación de vías de señalización neuroprotectoras por terapias basadas en estilos de vida y el aumento de resiliencia cerebral. Las moléculas clave de las vías de interés son especialmente sirtuína 1 y factores neurotróficos.

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