Biological mechanisms of generalised brain disease such as Alzheimer’s disease and schizophrenia

In a previous post, I discussed a theory concerning the causes of chronic brain diseases. This invoked the idea that the brain accumulated deleterious gene rearrangements during periods of rapid growth and remoulding, particularly those taking place at around 20 weeks of gestational age. The rate of mutation is enhanced by the action of reverse transcriptase that is heavily expressed during this period of neuronal division and synaptic pruning. The idea was that these somatic mutations might be propagated and increase the risk of diseases such as schizophrenia.

There was, however, a problem with the theory. How could a defect in one clone of neurones result in such a pervasive brain condition as schizophrenia or dementia? A possible mechanism is coming to light through the work of neuroanatomists who are using functional imaging on a massive scale to track previously invisible brain networks. This subject of ‘connectomics’ uncovers the networks through which disease may actually spread through the brain. It seems that the neurone malfunction can spread through the brain a little like a virus and perhaps the clue will come from the behaviour of infectious proteins such as those responsible for the spread of encephalopathies.¹ We shall see!

References
1.    Zhou J, Gennatas DE, Kramer JH, Miller BL, Seely WW. Predicting Regional Neurodegeneration from the Healthy Brain Functional Connectome. Neuron. 2012; 73:1226-1227