The past several decades has seen huge leaps in the understanding of neurological disease. Alzheimer's, schizophrenia, Parkinsons, Multiple sclerosis and others have been narrowed down to dysfunction of specific brain regions. What we still barely know, however, is how these regions are damaged in the first place. Parkinson's is caused by damage or decrease in substantia nigra dopamine neurons, but what causes this damage? Sadly, there is no real definitive answer as of yet. Genetics tends to be a factor, but hardly explains every case. Toxins or immunity may play a role, but they too can not fill in all of the blanks.
Viruses have long been known to cause neurological illness, but only a diminishing fraction of all viral infections are those of the brain. Viral encephalitis is a clear case off a viral brain infection marked by inflammation and occasionally fatal inter-cranial pressure. while encephalitis is an obvious brain infection recent research has indicated viruses to be much more neurologically active than we give them credit for.
Many viral infections of the brain have long been nigh impossible to understand. Diseases have long been defined as caused by specific factors, the flu causes the flu and so forth, but many viruses do not exhibit this behavior in the brain. The polio virus can infect the majority of the population, but only a portion are afflicted with motor impairment. Why this is little understood, it is clear that viruses can penetrate the blood brain barrier in infrequent events. These viruses can gain access by stowing away inside immune cells or lapse in barrier integrity.
More and more evidence is coming to light that potential viral brain diseases are not caused by a specific virus, but by the location that the virus is dispersed. viruses that find themselves in a specific structure can cause focal damage to that area. Infection of oligodendrocytes in mice has proven to show MS symptoms, however, it is not clear if damage is caused by viral lytic effects or the immune response to the infected cells. The VSV virus has been shown to indirectly destroy serotonin neurons in rodents. After infection microglia detect the infected neurons and destroy them with the virus inside, leaving no evidence that the virus was ever there. The only real indication of this virus is the later deficiency of serotonin neurons, but there is no indication why they are missing.
As can be seen in the case of VSV viruses can be silent neuron assassins, leaving no trace as to the origins of neuronal demise. While it is difficult to detect any presence of viral infection in the brain, this very nature indicates that they may lead to many neurological diseases. The selective and silent nature of these neuron killers make them a perfect candidate for diseases of specific damage.
van den Pol, Anthony N. Viral Infection Leading to Brain Dysfunction: More Prevalent Than Appreciated? Neuron doi:10.1016/j.neuron.2009.09.023 (volume 64 issue 1 pp.17 - 20)