The Axons of Evil

31. July 2009

When brain areas have decided on corporate tasks they discharge their action potential mostly synchronically. Their connective axes are not only made for data exchange – they also work as a gateway for Alzheimer & friends.

Several hundred billions of ways with each thousands of branches and crossways make the connection to important neighboring and also far away information distribution spaces. In split seconds important data reaches from sentries in the orbit to strategic control centers and on to the command centers responsible for orders to the outposts. Last year DocCheck covered the trial to create a ‘street map’ of the brain’s network. And a few weeks ago, the renown professional magazine “Neuron” published information that the main traffic axes between the relevant junctions in the central nervous system not only serve as data highways but also as road signs for demolition commands for neurodegenerative diseases.

Five diseases – five networks

Networks in the brain stand out due the associated neurons fire synchronically – and not only during the reaction to a stimulus but also during state of rest if they are “without task“. By these characteristics brain areas in men and apes can be determined which are connected with each other via nerve tracts. William Seeley and his colleagues in Stanford/California as well as Michael Greicius from San Francisco show now by aid of functional magnetic resonance: Alzheimer, but also other neurodegenerative disorders such as for example the behavioral variation of the front temporal dementia (bvFTD), at least in the “early-onset” state in the age of around 60 perform their work of destruction along those networks.

In an editorial Marsel Mesulam, Chicago, describes several examples of such networks. The most likely best examined is the front parietal network of selective visual attention which connects regions in the frontal visual field and in the lower parietal lobe controlling incidents in the room and their reaction to those. Since in addition to those two centers, other regions are connected, signals can get from one end of the data highway to the other via several different roads – which enables a flexible answer to larger amounts of information as well.

Neurologists were able to show in earlier studies already that the destructions during Alzheimer expand along those tracts. Seeley now picked five diseases which destroy more and more brain substance in the course of time. He then compared the regions with an increasing atrophy with his controls of healthy patients. Synchronous BOLD-frequencies (variances in the share of oxy-hemoglobin measured with magnetic resonance, therefore blood-oxygen-level-dependency) during the “task-free” state indicated the connected areas in his experiments.

In those studies, each of the examined diseases marked a network which is found in healthy people as well. For example Alzheimer corresponds closely with the “Default Mode Network” which is important in the creation of the episodical memory. But Seeley found even more: Not only the expansion of diseases corresponds with the roads of information in the brain but also the “population density”. In a healthy test person very similar densities of grey substance turn up in the different networks, i. e. neural cell bodies. Thus he confirmed again indications that synchronic firing of neurons stimulates the new creation of synapses in the according areas of a network.

Roads for messengers, viruses, prions and poisons

But what do those results means now? Networks in the brain not only transport data but also serve as roads for messengers (such as Nerve Growth Factor NGF), viruses, (polio) or toxins (tetanus). Also prion-diseases “wander” along the residues on those roads. Whether the disease chooses a “weak spot” in the brain as its square one and then makes its way hand over hand along these easily destructible targets or other – it’s not clear yet. Especially areas with a high density of nerve connections are significantly more sensitive against amyloid-plaque in Alzheimer patients and thus a malfunction. Perhaps it is enough to just clip network connections to get centers on “the other side” to degenerate. Each examined disease had selected its own “target area” and damaged another network during these studies.

And what about practical applications? The one knowing the criteria – how neurodegenerative diseases select their ‘square one’ to start spreading from there – definitely has a whole lot more possibilities to observe them in an early stage. That would be a first step towards a targeted therapy on time. Until then the observations from California are waiting for confirmation in other studies. Seeley and Greicius are for example considering prospective screening of younger test persons with a genetic risk factor for Alzheimer or front temporal dementia. In any case various areas of the central nervous system are connected possibly not only with tracts for data transfer. Despite their remarkable distances they rather form a community of fate in good times as in bad. The authors of the article put it as follows: “It seems that regions which fire at one go also grow together or perish”.

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