Insight into Neurodegenerative Disorder Using Melanocytes as a Model System

Abstract

Background: Neural crest cells (NCCs) by responding to several signals and paracrine factors get differentiated into different lineages like peripheral nervous system (PNS), chondrocytes, myofibroblast, endocrine, melanocytes, etc., Melanocytes are pigment-producing cells that share a common origin, paracrine factors (Wnt, FGF, and BMP), and transcription factors (TFs) with the neurons of the nervous system.

Objective: Neuronal model for neurodegenerative disorders are limited because of their nonhuman origin and transformation. In this review we propose the use melanocyte as a model system to study neurodegenerative studies.

Method: Systematic Literature Review.

Results: The similarity between neural crest-derived melanocytes and neurons, makes melanocyte an important model to study several neurodegenerative disorders like Alzheimer's disease and Parkinson's disorder.

Conclusion: Melanocytes and neurons share common origin i.e. both arise from NCC and share identical signalling molecules and pathways. Neural crest-derived melanocytes can thus serve as a promising model system to study normal and pathological behaviour of less accessible neurons.

Keywords: Melanogenesis; neural crest; neurodegenerative disease; transcription.

Figure 1

Regulatory steps in neural crest formation (Spengler et al. Nature Review, 2008)

Figure 2

Illustration of the NCC migratory pathways and its association with cellular fate. The main cell types of NCCs migrating in the ventral migratory pathway include sensory, sympathetic and SCPs. SCPs are the cellular source for Schwann cells, melanocytes and endoneurial fibroblasts. SC, spinal cord; DM, dermomyotome; NCCs, neural crest-derived cell types (Figure taken from Ernfors et al. Experimental Cell Research, 2010)

Figure 3

Transcription factors and signals involve in neural crest cell differentiation (Figure taken from Ernfors et al. Experimental Cell Research, 2010)

Figure 4

Amyloid plaques and neurofibrillary tangles are the hallmarks of AD. Accumulation of these abnormal protein cause loss of cholinergic neurons and hence dementia (Figure taken from Crlo. Immunity and ageing 2012)