Default Mode Network. Implications in Alzheimer’s, schizophrenia and autism

Default Mode Network (DMN) can be defined as a baseline of neuronal activity [1] that occurs when the subject has thoughts that are not directed toward a goal. It was discovered from the degree of variation in oxygen consumption of a number of areas of the brain, which were activated when people did not think of “anything special” (this is important). Another factor that has been used to study this network is synchrony (the degree of coordination of the frequencies emitted by neurons as a consequence of their electrical activity). To make a comparison, imagine frequency radios emitting on the same channel (or in several that are coupled) and shoot off at the same time communicating on a large scale.

In the typical DMN experiment, subjects are asked to close their eyes and not think of anything special or particular, just to stay awake. Magnetic resonance imaging (or other techniques) are then taken of the brain in areas of interest. Subjects are then asked to perform a task that requires thoughts and/or behaviors directed toward a goal (an executive demand).

These are the zones that are activated in the “at rest” situation (DMN):

In the image we can see how, in addition, to the areas in dark blue there are more blurred strokes that connect these areas. They are tracts of white matter and help us understand that the networks of the brain are configured as networks of “small world”: centers distributed and connected on a large scale in the brain. These networks evolve with maturation, in the first years of life they do not present so much cohesion [2]. Among the zones that are activated are

 

–         The medial prefrontal cortex, an area in which Brodmann Area 9 and 10, among others, are located. These two areas have been related to representations of our personality and social cognition.

–        The precuneus (ventral), related to episodic memory, consciousness and self. Also with visuoconstructive abilities

–         The lower parietal lobe, related to language, body image and identification of emotions. Also with spatial representation.

When the activity of the brain is contrasted in both situations (when “we don’t think about anything” vs. when we have a thought directed towards a goal/problem resolution), we obtain an image similar to the one above. The blue zones correspond to zones activated when the person executes a task (Networking). The orange zones would be DMN. The interesting thing is that the execution in the executive task correlates with a correct activation of the work network (“blue”) and a correct attenuation (which does not become deactivation) of the DMN (“orange”). Do we have an example of the sought-after “double dissociation” in neuropsychology?

Can’t think of anything specific?

Actually, when the researcher asks a subject to not think about anything specific for a period of time, we do something. First of all, we do not lose consciousness of ourselves. In general, the subjects of experiments during this experimental condition have reported that they think of themselves (self, personality), of things they have to do (prospective memory) or of events that have happened to them (episodic memory). Even in abstract concepts (semantic concepts) that may or may not be connected.

How does DMN relate to Alzheimer’s?

Alzheimer’s is a neuronal disconnection syndrome. This disconnection affects small world networks and their large-scale communication. In the case of DMN, the integrity of the network is implicated by the deterioration of the posterior cingulate cortex and thus the connectivity between the medial frontal region and the lower parietal lobe. The consequence is an incorrect activation of DMN, but also the existence of  “longer” and therefore less efficient networks (it depends on the method with which the phenomenon is studied). Sporns [3] mentions that precuneus is also an area particularly vulnerable to amyloid protein deposition, and the lack of DMN integrity is a biomarker in Alzheimer’s disease.

The cognitive consequence of this is the inability to unite cognitive contents from the previous section: intentional search in memory, loss of spatial schemes -both corporeal and non corporeal-, loss of abstract concepts, loss of personality. All this in a progressive way.

What relationship does DMN have with schizophrenia?

Schizophrenia can be conceptualized as a syndrome of disconnection, disintegration and desynchronization. We can see it in front-temporal connections, due to structural deficits but also in connectivity in white matter on a large scale and in the networks of the small world. The “materialization” of this can be seen in different cognitive aspects. Not only in working memory. Also a disconnection of language (mutism, intrusion of ruminations during the execution of a task, echolalia, disintegrated speech, etc.), of personality, consciousness, thought or body scheme.

In schizophrenia there are also alterations in the effectiveness of large-scale brain networks. What is the effect on DMN? It is double. There is a deficit in the inhibition of DMN. And when there is an incorrect suppression of DMN, the “working” network does not function properly [4]. Hence, for example, the typical intrusions of some schizophrenics during the execution of ADLs could arise.

How does DMN relate to autism?

In autism, in general terms, we can say that there is also an incorrect suppression of DMN, in addition to a low general activity of this network and poor processes of self-referral. In addition, and unlike previous syndromes, there could be an opposite profile in which small world networks are overconnected, producing a non-differentiation of networks on a large scale. This generates a loss of integration of the processes in which they intervene.

To learn more:

[1] Raichle, M. E., MacLeod, A. M., Snyder, A. Z., Powers, W. J., Gusnard, D. A., & Shulman, G. L. (2001). A default mode of brain function. Proceedings of the National Academy of Sciences, 98(2), 676–682. doi:10.1073/pnas.98.2.676

[2] Fair, D. A., Cohen, A. L., Dosenbach, N. U. F., Church, J. A., Miezin, F. M., Barch, D. M., Raichle, M. E., et al. (2008). The maturing architecture of the brain’s default network. Proceedings of the National Academy of Sciences of the United States of America, 105(10), 4028–4032. doi:10.1073/pnas.0800376105

[3]Sporns, O. (2011) Networks of the Brain. Ed. MIT

[4] Whitfield-Gabrieli, S., Thermenos, H. W., Milanovic, S., Tsuang, M. T., Faraone, S. V., McCarley, R. W., Shenton, M. E., et al. (2009). Hyperactivity and hyperconnectivity of the default network in schizophrenia and in first-degree relatives of persons with schizophrenia. Proceedings of the National Academy of Sciences, 106(4), 1279–1284. doi:10.1073/pnas.0809141106