Página editada por Antonio L. Manzanero, profesor de la Facultad de Psicología de la Universidad Complutense de Madrid. España


Facultad de Psicología
Campus de Somosaguas
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Feel helpless against Alzheimer’s disease?

You can do something to help prevent it
Jan 10, 2018 / Lisa Genova


Sacha Vega/iStock

We should all feel empowered to take steps to keep our brains and bodies healthy, says neuroscientist and novelist Lisa Genova.

How many of you reading this would like to live to be at least 80 years old? I think we all have a hopeful expectation of living into old age. Now let’s project this thought out into the future, and imagine we’re all 85. Out of every two people, one of us probably has Alzheimer’s disease.

Maybe you’re thinking, “Well, it won’t be me.” OK, then, you’ll be a caregiver. In some way, this terrifying disease is likely to affect us all.

Part of the fear around Alzheimer’s stems from the sense that there’s nothing we can do about it. Despite decades of research, we still have no disease-modifying treatment and no cure. So, if we’re lucky enough to live long enough, Alzheimer’s appears to be our brain’s destiny.

But maybe it doesn’t have to be. What if I told you that we could change these statistics — perhaps change our brain’s destiny — without relying on a cure or advancements in medicine?

Before we get into this, let’s go over what we currently understand about the neuroscience of Alzheimer’s. The point of connection between two neurons, or nerve cells, is called the synapse. The synapse is where neurotransmitters are released, transmitting signals and enabling communication. It’s where we think, feel, see, hear, desire and remember — and it’s where Alzheimer’s happens.

During the information communication process, in addition to releasing neurotransmitters like glutamate into the synapse, neurons also release a small peptide called amyloid beta. Normally, amyloid beta is cleared away or metabolized by microglia, the janitor cells of our brains. While the molecular causes of Alzheimer’s are still debated, most neuroscientists believe the disease begins when amyloid beta begins to accumulate. If too much is released or not enough is cleared away, the synapse begins to pile up with amyloid beta. When this happens, it binds to itself, forming sticky aggregates called amyloid plaques.

If you’re 40 years old or older, this initial step into the disease — the presence of accumulating plaques — can already be found in your brain, but the only way to be sure of this would be through a PET scan. Otherwise, you’re not showing any impairments in memory, language or cognition … yet.

Scientists think it takes at least 15 to 20 years of amyloid plaque accumulation before it reaches a tipping point, which then triggers a molecular cascade that causes the clinical symptoms of the disease. Prior to the tipping point, your lapses in memory may include things like,”Why did I come in this room?” or “Oh, what’s his name?” or “Where did I put my keys?” Before you freak out because you’ve asked at least one of those questions in the last 24 hours, those are all normal kinds of forgetting. In fact, these examples might not even involve your memory — maybe you just didn’t pay attention to where you put your keys in the first place.

After the tipping point actually occurs, those glitches in memory, language and cognition are different. Instead of eventually finding your keys in your coat pocket or on the table by the door, you find them in the refrigerator — or you find them and you think, “What are these for?”

What happens when amyloid plaques accumulate and reach this tipping point? Our microglia janitor cells become hyper-activated, releasing chemicals that cause inflammation and cellular damage. Scientists think they might actually start clearing away the synapses themselves. A crucial neural transport protein called tau becomes hyperphosphorylated and twists itself into tangles, which choke off the neurons from the inside. By mid-stage Alzheimer’s, your brain is full of massive inflammation, tangles and cell death.

If you were a scientist trying to cure this disease, at what point would you ideally want to intervene? Many researchers are betting big on the simplest solution: keeping amyloid plaques from reaching a tipping point. As a result, drug discovery is largely focused on developing a compound that will prevent, eliminate or reduce amyloid plaque accumulation. Which means the cure for Alzheimer’s will likely be a preventative medicine. We’ll need to take a pill before we reach the tipping point, before the cascade is triggered, before we start leaving our keys in the refrigerator. That may be why, to date, these kinds of drugs have failed in clinical trials — not because the science wasn’t sound but because the people in these trials were already symptomatic. It was too late.

Think of amyloid plaques as a lit match. At the tipping point, the match sets fire to the forest. Once the forest is ablaze, it doesn’t do any good to blow out the match. You must blow out the match before the forest catches fire.

This is actually good news for us, because it turns out the way we live can influence the accumulation of amyloid plaques. There are things we can do to keep us from reaching the tipping point. Picture your risk of Alzheimer’s as a seesaw scale. Pile risk factors on one arm of your seesaw, and when that arm hits the floor, you are symptomatic and diagnosed with Alzheimer’s. So, let’s imagine you’re 50 years old. You’re not a spring chicken anymore, so you’ve accumulated some amyloid plaques with age. Your arm is tipped a little bit.

We’ve all inherited DNA from our moms and our dads, and some of our genes will increase our risk and others will decrease it. If you’re like the character Alice in my book Still Alice, you’ve inherited a rare genetic mutation that cranks out amyloid beta, which will tip your seesaw arm to the ground.

But for most of us, the genes we inherit will tip the arm only a bit. For example, the gene variant increases amyloid, but you can inherit a copy of APOE4 from Mom and Dad and still never get Alzheimer’s. That means for most of us, our DNA alone does not determine whether we get Alzheimer’s. So what does?

Sleep could be a factor. In slow-wave deep sleep, our glial cells rinse cerebrospinal fluid throughout our brains, clearing away metabolic waste that accumulated in our synapses while we were awake. Deep sleep is like a power cleanse for the brain, and a single night of sleep deprivation can lead to an increase in amyloid beta. At the same time, amyloid accumulation has been shown to disrupt sleep, which in turn causes more amyloid to accumulate. So there’s a positive feedback loop that’s going to accelerate the tipping of the seesaw. Some scientists even believe poor sleep hygiene may be a predictor of Alzheimer’s.

Cardiovascular health is another factor. High blood pressure, diabetes, obesity, smoking and high cholesterol have all been shown to increase the risk of developing Alzheimer’s. Some studies have shown that as many as 80 percent of people with Alzheimer’s also had cardiovascular disease. Aerobic exercise has been shown in numerous animal studies to decrease amyloid beta. A heart-healthy Mediterranean lifestyle and diet may be able to help counter the tipping of this scale.

There are many things we can do to try to prevent or delay the onset of Alzheimer’s, but maybe you haven’t done any of them. Let’s say you’re 65; there’s Alzheimer’s in your family, so you’ve likely inherited a gene or two that tips your scale arm a bit; you’ve been burning the candle at both ends for years; you love bacon; and you don’t run unless someone’s chasing you.

Let’s imagine that your amyloid plaques have reached that tipping point. Your scale arm has crashed to the floor. You’ve set fire to the forest, causing inflammation, tangles and cell death. You should be symptomatic for Alzheimer’s. You should be having trouble finding words and keys. But you might not be.

There’s one more thing you can do to protect yourself from experiencing the symptoms of Alzheimer’s, and it has to do with neural plasticity and cognitive reserve. Remember, having Alzheimer’s is ultimately a result of losing synapses. The average brain has over 100 trillion synapses, which is fantastic; we’ve got a lot to work with. And this isn’t a static number. We gain and lose synapses all the time, through a process known as neural plasticity. Every time we learn something new, we are creating and strengthening new neural connections, new synapses.

In the Nun Study, 678 nuns, who were all over the age of 75 at the beginning of the study, were followed for more than two decades. They received regular physical checkups and cognitive tests, and when they died, they all donated their brains for autopsy. In some of these brains, scientists discovered something surprising. Despite the presence of plaques, tangles and brain shrinkage — what appeared to be unquestionable signs of Alzheimer’s — the nuns who possessed these brains had showed no symptoms of having the disease while they were alive.

Scientists think these nuns had a high level of cognitive reserve — meaning they had more functional synapses. People who have more years of formal education, who have a high degree of literacy, who regularly engage in mentally stimulating activities, all have more cognitive reserve. They have an abundance and a redundancy in neural connections. Even if they have a disease like Alzheimer’s compromising some of their synapses, they’ve got many extra backup connections, which buffers them from noticing that anything is amiss.

Why does this matter? I’ll give you a simplified example. Let’s say you only know one thing about a subject, and the subject is me. You know I wrote the novel Still Alice, and it’s the only thing you know about me. You have that single neural connection, that one synapse. Now, imagine you have Alzheimer’s. You have plaques, tangles, inflammation and microglia devouring that synapse. When someone asks you, “Hey, who wrote Still Alice?” you can’t remember, because that synapse is either failing or gone.

But what if you had learned more about me? Perhaps you learned four things about me. Now, imagine you have Alzheimer’s, and three of those synapses are damaged or destroyed. However, you still have a way to detour the wreckage; you can still remember my name.

We can be resilient to the presence of Alzheimer’s through the recruitment of yet-undamaged pathways. And we can start to create these pathways, this cognitive reserve, by learning new things. Ideally, we want these new things to be as rich in meaning as possible, recruiting sight, sound, associations and emotion.

This doesn’t mean doing crossword puzzles — you don’t want to simply retrieve information you’ve already learned. That’s like traveling down old, familiar streets, cruising neighborhoods you already know. You want to pave new neural roads. Building an Alzheimer’s-resistant brain could mean learning to speak Italian, meeting new friends, reading a book, or listening to a great TED Talk.

And if — despite all of your efforts — someday you are diagnosed with Alzheimer’s, there are lessons I’ve learned from my grandmother and the dozens of people living with this disease whom I’ve come to know. Being diagnosed with the disease does not mean you’re dying tomorrow, so keep living. You won’t lose your emotional memory. You’ll still be able to understand love and joy. You may not remember what you read five minutes ago, but you’ll remember how it made you feel. And you are more than what you can remember.

About the author

Lisa Genova is a neuroscientist and a novelist. Her writing explores the lives of people living with neurological diseases and disorders. A bestselling author, one of her novels was adapted into the Oscar-winning film, Still Alice.

La niña que jamás olvidaba una cara

Un estudio descubre las capacidades extraordinarias de una menor para el reconocimiento de rostros
Javier Salas
18 DIC 2017
La niña mostraba su capacidad ya antes de cumplir los 14 años.
La niña mostraba su capacidad ya antes de cumplir los 14 años.
Durante años, su familia notó que tenía un don. Podía reconocer por la calle sin problemas a alguien que había visto cuando solo tenía cinco años, incluso aunque hubiera cambiado considerablemente de aspecto con el tiempo. Viendo la tele, identificaba a quienes cruzaban fugazmente la pantalla como personas que se había encontrado anteriormente en un día cualquiera. Su madre, impactada por esta facultad inusual, decidió poner a su hija en manos de la ciencia. Así es como conocimos a O. B., la adolescente británica con el superpoder de reconocer rostros.
La madre de O. B. tocó la puerta del laboratorio de Sarah Bate, una especialista en la materia a quien había visto en los medios hablando de su trabajo para seleccionar policías con esta habilidad para las caras. Bate se puso de inmediato a trabajar para conocer si esta muchacha, que entonces tenía 14 años, era realmente una súper-reconocedora, como les llaman. Tras una serie de experimentos, comparando sus resultados con otras chicas de su edad y adultos con el don de los rostros, Bate no tuvo dudas: "El rendimiento de O. B. en múltiples tareas sugiere que ella es una súper-reconocedora: la más joven reportada hasta la fecha".
La capacidad de reconocer caras la damos por hecha, sobre todo las familiares, pero como explica Bate se trata de una capacidad cognitiva que se mueve en un amplio espectro, desde estos superdotados hasta los inquietantes casos de prosopagnosia, esa condición que impide prácticamente reconocer a nadie y que fue popularizada por el gran divulgador Oliver Sacks en El hombre que confundió a su mujer con un sombrero.
En las pruebas, la adolescente logró resultados comparables a los de los escasos súper-reconocedores adultos conocidos. Y en algunas hasta superó esas marcas. Además de por las buenas notas, el desempeño de O. B. permite hacerse una mejor idea de lo que implica esta aptitud. La muchacha tenía un cociente intelectual normal y no se podía considerar extraordinariamente capaz en ningún otro aspecto. Es más, como sucede en los adultos con su don, sus puntuaciones eran normales memorizando objetos, manos o rostros invertidos. Tampoco destacó identificando emociones en las caras. Ella solo tiene un poder: grabar en su memoria las facciones de la gente.
"Descubrimos que ella mira principalmente al centro de la cara, particularmente alrededor de la región de la nariz", explica Bate, que es el mismo truco que usan todos estos superdotados de forma espontánea. "Estos individuos muestran una estrategia visual especial para la percepción de rostros, para ver las características juntas como un todo, más que de manera fragmentada", indica la investigadora. Buena parte de este don se explica porque en lugar de mirar a los ojos hacen un escaneado más lento, centrándose en el centro de la cara, "punto focal óptimo para el procesamiento integral, lo que les permite reunir información de identidad de la manera más eficiente y precisa posible", según Bate.
Hasta la fecha, la ciencia solo había reportado este don en adultos y se desconocía si la capacidad se puede detectar antes en el desarrollo, explica Bate, que tuvo su primer encuentro con la niña superdotada hace un par de años, aunque es ahora cuando ha publicado junto a su equipo su estudio en Cognitive Neuropsychology. La investigadora de la Universidad de Bournemouth está buscando ahora casos entre niños más pequeños, para descubrir a qué edad temprana se puede adquirir esta madurez para los rostros.
Los científicos todavía se preguntan si reconocer y leer rasgos en las caras es una capacidad innata o adquirida. Recientemente, unos investigadores criaron a macacos hasta un año de edad sin ver caras, ni de humanos ni de congéneres, para adivinar cuánto de innato hay en la maquinaria de los primates para procesar rostros. El resultado fue sorprendente: los macacos desplazaron esa atención hacia las manos, que se convirtieron en el objeto más expresivo e interesante que conocían.
O. B. tiene una hermana, pero ni ella ni nadie más en su familia tiene estas habilidades, a pesar de que se sabe que es una condición bastante heredable. Por ejemplo, se sabe que la prosopagnosia (la ceguera para las caras) es un trastorno que se puede repetir dentro de la misma familia. Y los gemelos idénticos comparten más las mismas capacidades que los que no lo son. Además, se ha comprobado que no es una habilidad que se pueda mejorar mucho con el entrenamiento: el personal que lleva años trabajando en el control de pasaportes no es mucho más capaz que un empleado recién llegado al puesto.
Bate también se dedica a ayudar a la policía metropolitana del Reino Unido a seleccionar a agentes con estas dotes. "Conocí a un oficial que había visto un retrato robot construido por un testigo ocular y un tiempo después arrestó a alguien por otro crimen. Pensó que se parecía al de aquel retrato ¡y resultó que el sospechoso era responsable del crimen anterior!", cuenta la especialista. Reivindica que estos agentes pueden ser de gran utilidad, sobre todo porque los sistemas basados en inteligencia artificial todavía fallan bastante cuando las condiciones no son óptimas, que suele ser lo habitual. Estos agentes han servido para capturar criminales, para reconocer abusadores sexuales en la multitud y también para dar con personas perdidas en el caos posterior a una catástrofe, asegura Bate. No todos los superhéroes llevan capa.

Nuevo número del Anuario de Psicología Jurídica 2017

Vol. 27. Núm. 1. 2017 Páginas 1-130
El sexismo como predictor de la violencia de pareja en un contexto multicultural
Ainara Arnoso, Izaskun Ibabe, Maitane Arnoso, Edurne ElgorriagaAnuario de Psicología Jurídica 27 (2017) 9-20Resumen - Texto Completo - PDF
Modelo ENCUIST: aplicación al perfilado criminal
Lucía Halty, José Luis González, Andrés SotocaAnuario de Psicología Jurídica 27 (2017) 21-31Resumen - Texto Completo - PDF
Agresores sexuales juveniles: tipología y perfil psicosocial en función de la edad de sus víctimas
Carlos Benedicto, David Roncero, Luis GonzálezAnuario de Psicología Jurídica 27 (2017) 33-42Resumen - Texto Completo - PDF
Análisis comparativo de la percepción de la conducta violenta grupal por parte de jóvenes agresores y no agresores residentes en la Comunidad de Madrid (España)
María Jesús Martín, José Manuel Martínez, Rubén García-Sánchez, Begoña Aramayona, Carmen Almendros, Cristina JiménezAnuario de Psicología Jurídica 27 (2017) 43-50Resumen - Texto Completo - PDF
Propiedades psicométricas del cuestionario de personalidad EPQ-A en una muestra de adolescentes hispanohablantes
Miguel Ángel Alcázar-Córcoles, Antonio Verdejo-García, José Carlos Bouso-Sáiz, Javier Revuelta-Menéndez, Ezequiel Ramírez-LiraAnuario de Psicología Jurídica 27 (2017) 51-6Resumen - Texto Completo - PDF
Psychopathy: Legal and neuroscientific aspects
Joaquin Ortega-Escobar, Miguel Ángel Alcázar-Córcoles, Leopoldo Puente-Rodríguez, Enrique Peñaranda-RamosAnuario de Psicología Jurídica 27 (2017) 57-66Resumen - Texto Completo - PDF
Escala de Gravedad de Síntomas del Trastorno de Estrés Postraumático según el DSM-5: versión forense (EGS-F)
Enrique Echeburúa, Pedro J. Amor, José Manuel Muñoz, Belén Sarasua, Irene ZubizarretaAnuario de Psicología Jurídica 27 (2017) 67-77Resumen - Texto Completo - PDF
Stability of autobiographical memory in young people with intellectual disabilities
Claudia Morales, Antonio L. Manzanero, Alina Wong, Mar Gómez-Gutiérrez, Ana M. Iglesias, Susana Barón, Miguel ÁlvarezAnuario de Psicología Jurídica 27 (2017) 79-84Abstract - Full text - PDF
Age-related differences in the phenomenal characteristics of long-term memories of March 11, 2004 terrorist attack
Rocío Vallet, Antonio L. Manzanero, Javier Aróztegui, Rubén García ZurdoAnuario de Psicología Jurídica 27 (2017) 85-93Abstract - Full text - PDF
Cognición, emoción y mentira: implicaciones para detectar el engaño
Iris Blandón-Gitlin, Rafael M. López, Jaume Masip, Elise FennAnuario de Psicología Jurídica 27 (2017) 95-106Resumen - Texto Completo - PDF
Custodia compartida, corresponsabilidad parental y justicia terapéutica como nuevo paradigma
Francisca Fariña, Dolores Seijo, Ramón Arce, Ma José VázquezAnuario de Psicología Jurídica 27 (2017) 107-13Resumen - Texto Completo - PDF