With cillary diseases being investigated has there ever been any done on the loss of smell accruing from parkinson's. Do they influence the passage of meds via the olfactory route. Anyone know where I can find more info?





Hypomorphic CEP290/NPHP6 mutations result in anosmia caused by the selective loss of G proteins in cilia of olfactory sensory neurons.

DP McEwen, RK Koenekoop, H Khanna, PM Jenkins, I Lopez, A Swaroop, JR Martens
Departments of Pharmacology, Ophthalmology, and Human Genetics, University of Michigan, Ann Arbor, MI 48105.

Cilia regulate diverse functions such as motility, fluid balance, and sensory perception. The cilia of olfactory sensory neurons (OSNs) compartmentalize the signaling proteins necessary for odor detection; however, little is known regarding the mechanisms of protein sorting/entry into olfactory cilia. Nephrocystins are a family of ciliary proteins likely involved in cargo sorting during transport from the basal body to the ciliary axoneme. In humans, loss-of-function of the cilia-centrosomal protein CEP290/NPHP6 is associated with Joubert and Meckel syndromes, whereas hypomorphic mutations result in Leber congenital amaurosis (LCA), a form of early-onset retinal dystrophy. Here, we report that CEP290-LCA patients exhibit severely abnormal olfactory function. In a mouse model with hypomorphic mutations in CEP290 [retinal dystrophy-16 mice (rd16)], electro-olfactogram recordings revealed an anosmic phenotype analogous to that of CEP290-LCA patients. Despite the loss of olfactory function, cilia of OSNs remained intact in the rd16 mice. As in wild type, CEP290 localized to dendritic knobs of rd16 OSNs, where it was in complex with ciliary transport proteins and the olfactory G proteins Golf and Ggamma13. Interestingly, we observed defective ciliary localization of Golf and Ggamma13 but not of G protein-coupled odorant receptors or other components of the odorant signaling pathway in the rd16 OSNs. Our data implicate distinct mechanisms for ciliary transport of olfactory signaling proteins, with CEP290 being a key mediator involved in G protein trafficking. The assessment of olfactory function can, therefore, serve as a useful diagnostic tool for genetic screening of certain syndromic ciliary diseases.

cillary diseases loss of smell parkinson's medications olfactory route
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Guy

our sense of smell is because we have a depletion of the mineral zinc,
however essential oils can be very healing as well -they unlock many things in the brain, I use them rose, lavender, and orange, etc. quite a bit


http://home.iprimus.com.au/rboon/EssentialOils.htm

The Olfactory System

The olfactory system is one of the first nerve systems to develop completely in the human being. During the seventh week of gestation, the embryo develops remarkably. It is during this period of growth that the telencephalon (the most forward part of the embryonic brain) develops the olfactory lobes which ultimately produce the riencephalon (the limbic lobes which process our olfactory sense). The riencephalon is the oldest part of the brain phylogenetically, and is that part of the brain that is the seat of our emotional selves. Thus we can see the intimate connections between the olfactory system and our emotions.

The olfactory bulb is the first place that Lewy bodies show up. We typically lose our sense of smell as much as 20 to 30 years before other symptoms show up.

The next place the Lewy bodies appear is in the stomach wall. That hints at something that we breathe in and then sinus drips on down. My bets are on LPS laden house dust giving our immune system fits which our endocrine system seeks to counter with cortisol.