From A Matter of Balance:
"A report in today’s Science Daily discusses the loss of smell as the result of viral infections. And, while seemingly not realized by the authors, it leads to a posssible avenue for PD treatment using a very old drug.

According to the research of the German scientist Braak, one of the first places that Lewy bodies, the purported “footprints” of Parkinson’s Disease, are found is in the olfactory bulb. Directly connected to the environment via the nasal cavaties, this provides an obvious path for pathogens and toxins which may play a role.

Further, the loss of a sense of smell is often the first symptom of PD and can precede other effects by as much as twenty years.

Given its central location in the PD landscape, anything which restores the sense of smell holds great interest. If it can do that, can it do more?

The article, entitled “Study Examines Treatment For Olfactory Loss After Viral Infection”, examines the work of a Korean team led by Beom Seok Seo, M.D., of Seoul National University College of Medicine. While no mention is made of PD, there are none-the-less some interesting implications.

For one, the article points out that infection by a number of viruses can cause the loss of the sense of smell, including influenza. Coming so close behind the St. Jude’s work showing that the same viruses can trigger activation of microglia and lead to the same type of damage associated with PD, the idea of neuroinflammation as a factor continues to gain credence.

The Korean study lent even more weight when they found that the use of glucocorticoids as well as ginkgo was able to partially correct that loss. Both substances are powerful anti-inflammatories.

An earlier report discusses the widespread loss of olfaction among welders, a group at high risk for PD.

So, given the recurring role of this symptom, yet a third article about the ability of an old asthma drug called theophyline to restore the sense of smell caught my eye.

“The drug theophylline is a generalized phosphodiesterase inhibitor. Physicians have determined that the drug is a generalized inhibitor which means it causes certain chemicals like cAMP and cGMP to increase. Thus, the higher the levels of cAMP the greater the ability to smell. This is true to a lesser extent for cGMP.”

So it increases the levels of cAMP. So what? Well, a great deal, actually. From yet another article in the same magazine:

“Increased amounts of the proteins were associated with a significant rise in the level of an important signaling molecule inside the nerve cells called cAMP. This molecule plays a key role in regulating nerve-cell growth, differentiation and survival, and the regeneration of long parts of the cell called axons that carry the nerve impulses.

Levels of cAMP drop in mammalian nerve cells as they mature, and this is thought to explain, in part, why mature nerve cells cannot regenerate damaged axons.

“Our findings provide additional evidence that cAMP plays an important role in axon growth and suggest that these receptors are likely to play a major role in regulating cAMP production in nerve cells,” says Saeki, an associate professor of neurological surgery and chief of Ohio State’s Dardinger Laboratory for Neuro-oncology and Neurosciences.”

Medline lists a handful of studies on the short term effects of the drug on PD symptoms, mainly a lengthened “On” time, but none on the bigger question of neurogenesis.