Loss of Sence of Smell
 

I have read that loss of sence of smell can be many years prior to other symptoms in 70-80% of Parkinsons patients.

Does anyone have any insight as to why it is not across the board. If olfactory system is said to be first affected area of brain, why would it not be across the board?

Yet another thing scientists don't know, but there are ongoing biomarker studies testing sense of smell of pwp and controls - my husband & I are in two of these studies.

Jean

One possibility is that we are talking about two or more different diseases. Another is that there is some variable involved.

My own view- While the sense of smell is touted as the first symptom, that is not quite true. It depends on if you mean the first one noticed by the patient or the first one that can be detected by scientists.

If the latter, there seems to be a tie of sorts between the olfactory bulb and the nerves found in the wall of the stomach (the myenteric plexus). These are the first places that German researcher Braak found Lewy bodies appearing.

These two areas share a common trait - they are in intimate contact with the outside world. We breathe in things that stick to our sinuses. Most are swept out, a few penetrate the defenses in that area, and the rest end up in the stomach. Something in the environment. It is airborne (else the olfactory bulb would not be affected). It is probably a pollutant that came with industry.

It is also probably a "secondary" factor in that it spells trouble only for those already predisposed (else more would be affected). And it should be capable of moving along the axons to match Braak's other observations. This means it has to be tiny particles or even molecules.

Although researchers haven't caught on yet, there is an ideal candidate available. Soot. Or, if you prefer, Ultra-Fine Particulates. Produced by burning diesel, coal, charcoal, etc. these tiny specks of matter can penetrate deeply and pass through most barriers. They are also capable of acting as ferries and carrying toxins with them. If inhaled by a person who already has an inflammation-prone system, the resulting inflammation allows even deeper penetration while also revving up the host's immune response.

most interesting
 

Ron,

My mom was a smoker my whole life long. Plus I had a bad case of Valley Fever at age 16 (a lung infection from airborne fungus -- when dust around construction areas and agricultural areas is transported by the wind). Maybe either or both fit your hypothesis?

Jean

Yes, Jean, any thing that would stimulate the immune response would contribute to some degree or another. Once the hypersensitivity is in place, dozens of environmental factors become potential "causes". As if that were not bad enough, some of them synergize with one another.

While all this is building up, our endocrine system is pumping out steroids to quell the inflammation. But, because our immune system is sensitized it doesn't go into a full stand down mode and is ready to resume the inflammatory response on a moment's notice. We end up on a destructive see-saw.

Uncanny timing...
 

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