I happen to fall into the 20-30% bracket who can still smell. I think this is indicative of the fact we all have varying disease etiologies or pathologies involved in other words, "this isn't your grandmother's PD" we're looking at. Different triggers but same output - a cluster of symptoms from brain damage with cardinal signs that conform to PD. It is now recognized that PD may be a continuum or spectrum of several disorders.

I just so happened to finish reading an interesting article in Brain (full text and free to boot); we must have similar biorhythms this week or something.

Olfactory dysfunction, central cholinergic integrity and cognitive impairment in Parkinson's Disease. Bohnen et al. 2010:133 (6).

The finding is that a smell impairment has more correlation to the loss of acetylcholine, not dopamine. This, is to me at least, further proof that we are all hit by this thing the medical establishment continues to call PD. As Rick just posted, there are many ways to get to manifesting the same cardinal signs, but clearly there should be more than approach to understanding it and treating it. It is believed that acetylcholine transmission is hit early on before dopamine involving the archicortex of the limbic system.

Here are a few facts I learned:

Researchers and clinicians have known for over 30 years that PWP lose a sense of smell long before motor symptoms appear.

Anosmia also occurs in Alzheimer's Disease and is more strongly linked to presence of Lewy Bodies.

Strong correlation between cognitive impairment and may be linked to dementia.

Note that there are cases where PWP present early on with hypernosmia, or smelling things that are not detected by others. These could be smells that are detectable but in the PWP are overpe

Hmmm...it's only taken 30 years to begin researching anosmia in earnest as a viable biomarker for PD. If it is essentially key to the development of a form of PD, then I would think it more important to study how the disease burrows in and takes hold of the brain as a way to stop it, rather than refining how to use it as a test for the disease. Maybe there should start to be some focus on how perhaps this type of PD, AD, and Lewey Body Disease (Anosmic variety is now a bonafide phenotype of AD) may have a very common pathophysiology at the very beginning but rather branch out to other neurodenerative pathways (one sticks with acetycholine, while the other then moves on to dopamine).

Will it ever be recognized by the research community that perhaps in studying how the ways ways we diverge from one another and that these sorts of back door connections may just provide the one key we need to unlock the door to understanding how neurodegenerative diseases take root in the first place?

Laura