Following on from Richard's post the other day, this is a really nice study looking at the association between smell loss/deficit and risk of PD. Although this is a well established link, there are actually relatively few cohort studies that have assessed smell objectively in a large number of participants and followed them up for a sufficient duration of time.
The method of ascertaining may, as the authors point out, result in a smaller number of incident cases, which will lead to conservative estimates as long as the ascertainment does not differ between the different levels of smell. However, the method of ascertainment may also lead to imprecise estimates of how long before a diagnosis of PD smell loss occurs. This time period is a really important thing to understand if it is to be used to determine who should participate in disease modifying trials.
The authors do however deserve great praise for undertaking a study that gives us gender specific estimates and estimates in the afro-carribean community...
Neurology. 2017 Sep 6. pii: 10.1212/WNL.0000000000004382. doi: 10.1212/WNL.0000000000004382. [Epub ahead of print]
Chen H, Shrestha S, Huang X, Jain S, Guo X, Tranah GJ, Garcia ME, Satterfield S, Phillips C, Harris TB; Health ABC Study.
Collaborators (9)
http://www.neurology.org/content/early/2017/09/01/WNL.0000000000004382
OBJECTIVE:
To investigate olfaction in relation to incident Parkinson disease (PD) in US white and black older adults.
METHODS:
The study included 1,510 white (mean age 75.6 years) and 952 black (75.4 years) participants of the Health, Aging, and Body Composition study. We evaluated the olfaction of study participants with the Brief Smell Identification Test (BSIT) in 1999-2000. We retrospectively adjudicated PD cases identified through August 31, 2012, using multiple data sources. We used multivariable Cox models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).
RESULTS:
During an average of 9.8 years of follow-up, we identified a total of 42 incident PD cases, including 30 white and 12 black participants. Overall, poor sense of smell, as indicated by a lower BSIT score, was associated with higher risk of PD. Compared with the highest tertile of BSIT (t3), the HR was 1.3 (95% CI 0.5-3.6) for the second tertile (t2) and 4.8 (95% CI 2.0-11.2) for the lowest tertile (t1) (ptrend < 0.00001). Further analyses revealed significant associations for incident PD in both the first 5 years of follow-up (HRt1/[t2+t3] 4.2, 95% CI 1.7-10.8) and thereafter (HRt1/[t2+t3] 4.1, 95% CI 1.7-9.8). This association appeared to be stronger in white (HRt1/[t2+t3] 4.9, 95% CI 2.3-10.5) than in black participants (HRt1/[t2+t3] 2.5, 95% CI 0.8-8.1), and in men (HRt1/[t2+t3] 5.4, 95% CI 2.3-12.9) than in women (HRt1/[t2+t3] 2.9, 95% CI 1.1-7.8).
CONCLUSIONS:
Poor olfaction predicts PD in short and intermediate terms; the possibility of stronger associations among men and white participants warrants further investigation.
© 2017 American Academy of Neurology.
An Australian paper some years ago concerned the harvesting of nasal olfactory cells as a base for production of stem cells. These nasal cells proved to be undamaged sshowing that the lack of olfaction is caused by damaged innervation rather than damaged olfactory cells. This accounts for the return of some degree of olfaction following the daily intake of palmitoyl ascorbate (ascorbyl palmitate or E-304) by people with Parkinson's. Simultaneously the Parkinson's symptoms of poor writing and speech are often improved as are balance and gait. This recovery indicates that the nerve damage is probably physiological and therefore reversible rather than terminal.
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