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Quadruple Immunostaining of the Olfactory Bulb for Visualization of Olfactory Sensory Axon Molecular Identity Codes
Published on: June 5, 2017
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The olfactory bulb proteotype differs across frontotemporal dementia spectrum
Mercedes Lachén-Montes1, Andrea González-Morales1, Domitille Schvartz2
1Clinical Neuroproteomics Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), Irunlarrea, 3, 31008 Pamplona, Spain; Proteored-ISCIII, Proteomics Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), Irunlarrea 3, 31008 Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain, Irunlarrea 3, 31008 Pamplona, Spain.
Journal of Proteomics
|April 19, 2019
Summary
Frontotemporal dementias (FTD) involve olfactory dysfunction due to molecular changes in the olfactory bulb (OB). This study reveals distinct protein alterations in progressive supranuclear palsy (PSP) and FTLD-TDP43, impacting survival pathways.
Area of Science:
- Neuroscience
- Proteomics
- Molecular Biology
Background:
- Mild olfactory dysfunction is a known symptom in frontotemporal dementias (FTD).
- The specific molecular mechanisms driving olfactory deficits in FTD subtypes remain unclear.
- Progressive supranuclear palsy (PSP) and frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP43) are clinically similar FTD disorders with distinct neuropathological features.
Purpose of the Study:
- To investigate the molecular differences in the olfactory bulb (OB) between PSP, FTLD-TDP43, and non-FTD individuals.
- To identify specific protein alterations and signaling pathway dysregulations in the OB associated with different FTD subtypes.
- To understand the role of the OB in the pathophysiology of FTDs.
Main Methods:
- Quantitative proteomics was employed to analyze olfactory bulb tissue samples.
- Samples were obtained from individuals with PSP, FTLD-TDP43, and age-matched non-FTD controls.
- Functional and pathway analyses were performed on the proteomic data.
Main Results:
- PSP cases showed mitochondrial and calcium homeostasis impairment in the OB.
- FTLD-TDP43 cases exhibited disruptions in protein synthesis and vesicle trafficking.
- Both FTD subtypes displayed altered olfactory mitogen-activated protein kinases (MAPKs), calcium/calmodulin dependent protein kinase II (CAMKII), and protein kinase C (PKC) signaling.
- PSP uniquely showed a shut-off in the mitogen-activated protein kinase kinase 4 (SEK1/MKK4)/stress-activated protein kinase (SAPK) axis.
- FTLD-TDP43 uniquely showed phosphoinositide-dependent protein kinase 1 (PDK1) inactivation.
Conclusions:
- This study reveals distinct molecular changes in the olfactory bulb associated with PSP and FTLD-TDP43.
- Shared alterations in survival signaling pathways were observed across both FTD subtypes.
- Specific pathway dysregulations highlight differences in the molecular pathophysiology of PSP and FTLD-TDP43 at the olfactory level.
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