Parkinson’s disease is the second most common cause of progressive NODs. Worldwide, 10 million people are affected by PD (http://​www.​pdf.​org/​en/​parkinson_​statistics.​2013). PD is characterized by the degeneration of nigrostriatal dopaminergic neurons Dirnberger and Jahanshahi, 2013. Extensive degeneration of dopaminergic neurons results in programmed cell death, viral infection and accumulation of environmental toxins Lang and Lozano, 1998. Hallmarks of pathogenesis are protein mis-folding and dysfunction of ubiquitin proteasome pathway. Lewy bodies formation occurs with α-synuclein and ubiquitin. Symptoms include bradykinesia, rigidity, resting tremor and postural instability. It is also associated with non-motor symptoms Dauer and Przedborski,2003.

Frontotemporal lobar degeneration (FTLD) and Amyotrophic lateral sclerosis (ALS) are most commonly overlapping neurodegenerative diseases. FTLD is a non-Alzheimer form of dementia characterized by either abnormal behavioral or aphasic patterns in people under the age of 65 years Neary et al., 1998. FTLD can be sporadic or familial. FTLD can occur independently or with combination of amyotrophic lateral sclerosis, Parkinson’s disease and with other neurodegenerative diseases Ratnavalli et al., 2002. Amyotrophic lateral sclerosis is a neurodegenerative motor neuron disease. It is also called as Lou Gehrig’s disease. It affects both upper and lower motor neurons. Upper motor neuron degeneration signs are hyperreflexia, extensor plantar response, increased muscle tone and weakness in topographic representation, while lower motor neuron degeneration signs comprise of weakness, muscle wasting, muscle cramps, fasciculation’s and hyporeflexia. Regardless of initial symptoms, it eventually results in muscle atrophy and weakness Hardiman et al., 2011. Death occurs within 3 to 5 years of diagnosis. Only 10% of ALS is familial, while 90% is sporadic. Genetic reasons for ALS still remain unclear AI-Chalabi et al., 2012.

FTLD and ALS are caused as a result of dysfunction of many proteins. Origin of these neuro-degenerative diseases are multifactorial, among the numerous proteins such as Tau, Tar DNA binding (TDP-43) protein and Fused in Sarcoma (FUS) protein dysfunctions are observed commonly in both FTLD and ALS. Biological properties of these proteins are different in normal and diseased conditions. For instance, in healthy people TDP-43 is localized in the nucleus and it plays a role in transcriptional regulation, pre-mRNA splicing, microRNA processing and mRNA transport (Buratti, 2(08). Contradictorily, in FTLD and ALS patients, TDP-43 proteins are present as aggregates in the cytoplasm.

Cells that possess the property of self-renewal and differentiation to multiple cell types are called stem cells. Stem cells are classified into the following types based on their ability to differentiate.

1) Totipotent stem cells, that differentiate to any type of cell (e.g. Embryonic four cell stage)

2) Pluripotent stem cells, that differentiate to many cell types (e.g. Embryonic stem cells)

3) Multipotent stem cells differentiation are limited to few cell types (e.g. Adult stem cells)

Induced Pluripotent cells (iPSCs). These cells are non pluripotent cells (somatic cells) which are induced to become pluripotent. This induction via regulating transcription factors such as Oct4, Sox2, Klf4 and c-Myc Eminli et al., 2008Okita et al., 2007Wernig et al., 2007

Embryonic stem cells (ESCs), Mesenchymal stem cells (MSCs) and Induced pluripotent stem cells (iPSCs) are transformed to neuronal progenitor cells (NPCs) or neuronal stem cells (NSCs) from which several neuronal lineages are obtained based on specific differentiation. Upshot is that, reprogramming the cell to various neuronal lineage to correct neurodegenerative diseases. Manipulating expression of the transcription factors will convert fibroblast cells to neuronal cells. Factors such as Asell, Brn2, and Myillin Pang et al.,2011 and Mashl, Ngn2, Nurrl and Ptx3 in Liu et al., 2012 reported to reprogram the cells to neuronal cells.

Induced pluripotent stem cells were used in developing cellular models. iPSCs were used to create models for AD Israel et al., 2012 PD (Woodard et al., 2014), ALS Egawa et al., 2012 and Huntington’s disease Juopperi et al., 2012. These models assist in understanding the pathological changes occurred during the disease progression. These changes could be of phenotypic or sub cellular observations Swinney and Anthony, 2011. Apart from developing cellular models, stem cells are used in two ways to treat neurodegenerative diseases. In first place, stem cells are "Necessary cell population" in transplanted affected region, where it is intended to replace the complete functionality of degenerated neurons. Secondly, stem cells are used as "Auxiliary cell population" to serve as a source to induce other cells via promoting the secretion of neuroprotective growth factors such as brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) Medvedev et al., 2010Suzuki and Svendsen, 2008Xuan et al., 2008. Figure 2 shows the application of stem cells in NDDs.

Representative studies of currently available studies in treating NDDs and potentiality of stem cell in treating NDDs have been tabulated in Table 1 .