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Neural Stem Cells for the Treatment of 7 Common Neurological Disorders

In recent years, neural stem cell (NSC) therapies have given hope to many patients with neurological damage. These abilities of NSCs can regenerate damaged nerve tissues. As a result, different clinical trials have been conducted to study the regenerative abilities of NSCs, some of which have shown great promise. These include the most common diseases such as stroke, traumatic brain injury, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, multiple sclerosis and spinal cord injury.

NSC plasticity and therapeutic use. (Ottoboni, Linda, et al., 2020)Fig. 1 NSC plasticity as a function of origin (x-axis) and therapeutic use (y-axis).1

Creative Biolabs summarizes current knowledge about NSC transplantation for neurodegenerative diseases. We are committed to elucidating the plasticity of NSCs to better exploit the potential of these cells. As a partner, we offer the following related services to help accelerate the progress of your NSC program.

Our Services Descriptions
Neural Stem Cell Differentiate Stem cells are regarded as an important tool for neurobiological research. Creative Biolabs provides customers with comprehensive primary stem cell extraction, isolation, and NSC differentiation services.
NSCs Differentiation Assay NSCs derived from neural tissue maintain stable biological properties, including differentiation capacity and histocompatibility, which have been applied in various aspects of research, treatment, and drug screening of neurological diseases. Creative Biolabs provides the most comprehensive NSCs differentiation assay to assist clients worldwide in research related to neurology.
Cell-depends Neurological Disease Solutions Cell therapy can provide protective and anti-inflammatory effects on neural tissue, as well as replace and repair damaged neurons and glial cells, thereby reducing inflammation, rebuilding functional circuits, and relieving symptoms. Creative Biolabs provides the most reliable and thorough one-stop solution for neurological diseases to our clients around the world.

The Potential of NSCs in Stroke Treatment

Stroke causes sudden neurological damage due to disruption of the cortical circulatory system. In addition to neuronal loss, the inflammatory response is heightened in acute stroke, leading to destruction of hypoxic tissue in the area of injury as well as the initiation of a cytokine cascade response that enlarges the damaged area.

Because of their neuroprotective, neurogenic, and immunomodulatory potential, NSCs have been heavily investigated as a potential therapeutic approach in numerous trials in either the acute or chronic phase.

  • The ability of NSCs to transport immunomodulatory and neuroprotective factors may reduce inflammation.
  • Administering NSCs in the chronic phase of stroke has been shown to activate regenerative mechanisms that may help restore brain function.

The Potential of NSCs in the Treatment of Traumatic Brain Injury

The most serious disease is traumatic brain injury (TBI), which can result in death or severe neurological damage. The damage from TBI can be divided into two phases. The early stage is a direct result of the initial injury and leads to rupture of the blood-brain barrier (BBB), brain edema, and cranial hemorrhage, which results in rapid cell death in the affected brain regions. The next phase is associated with the release of excitatory amino acids, ionic imbalances, calcium overload, mitochondrial dysfunction, and ongoing neurodegeneration. In addition, immune and inflammatory responses following brain injury increase neuronal death. Posttraumatic neuroinflammation occurs with the release of proinflammatory cytokines, migration of immune cells, and activation of microglia.

Previous studies have shown that:

  • Motor and cognitive deficits induced by traumatic brain injury in mice can be attenuated by injecting NSCs directly into the injured brain.
  • In addition, stem cell treatment of TBI animals can stimulate the damaged brain to produce trophic factors that reduce inflammation, and support neurogenesis, neuroprotection, and neuroregeneration.

The Potential of NSCs in Alzheimer's Disease Treatment

Alzheimer's disease (AD) is a common neurodegenerative disorder that can be recognized by cognitive decline, memory loss, disruptive behaviors, and aphasia. Pathogenic alterations in AD include abnormal beta-amyloid (Aβ) accumulation and aberrant phosphorylation of tau proteins, which leads to neuroinflammation that damages the central nervous system (CNS).

NSC transplantation may help AD patients improve cognitive deficits by reducing A deposition and rescuing memory problems.

  • In a mouse model of AD, NSCs were found to reduce A levels by promoting autophagy in damaged neurons.
  • This may be accompanied by upregulation of the levels of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and vascular endothelial growth factor (VEGF), which protect neurons and neuronal integrity in patients.

A number of antibodies are important tools commonly used in AD research. You can browse the table below to see a list of our recommended products.

Cat. No Product Name Clonality Applications
NRP-0422-P2292 NeuroMab™ Anti-Amyloid Beta 1-15 Antibody, Clone mAb158 Monoclonal Inhib; In Vitro; In Vivo
NRZP-1022-ZP2792 NeuroMab™ Anti-Amyloid Beta BBB Shuttle Antibody, Clone mAb158 Monoclonal Inhib; In Vitro; In Vivo
NRP-0422-P867 NeuroMab™ Anti-Amyloid Beta 1-15 Antibody, Clone Donanemab Monoclonal In Vivo
NRP-0422-P2275 NeuroMab™ Anti-Tau Antibody, Clone Alz50 Monoclonal WB; ELISA; In Vitro; In Vivo
NK-2106-P008 Tau Monoclonal Antibody (AT120, HT7 and BT2 clone) Monoclonal
NRP-0422-P1683 NeuroMab™ Anti-Tau Antibody, Clone HJ9.3 Monoclonal FC; ELISA; Inhib; In Vitro; In Vivo
NRP-0422-P1684 NeuroMab™ Anti-Tau Antibody, Clone HJ8.5 Monoclonal FC; ELISA; Inhib; In Vitro; In Vivo
NRP-0422-p1686 NeuroMab™ Anti-Tau Antibody, Clone HJ8.7 Monoclonal FC; ELISA; Inhib; In Vitro; In Vivo
NRP-0422-P1719 NeuroMab™ Anti-pTau Antibody, Clone PHF1 Monoclonal WB; IHC; ICC; In Vitro; In Vivo
NRP-0422-P2293 NeuroMab™ Anti-Tau Antibody, Clone 6C5 Monoclonal Inhib; Block; In Vitro; In Vivo
NAB-0720-Z6479 NeuroMab™ Mouse Anti-LRP1 Monoclonal Antibody (CBP3363) Monoclonal IHC-Fr; IHC-P; WB; ICC; IF; FC;  EMDB;
NRP-0422-P792 NeuroMab™ Anti-TREM2 Antibody, Clone NR65P Monoclonal FC; ELISA; In Vitro; Agonist; In Vivo
NRP-0422-P1220 NeuroMab™ Anti-EPHB2 Antibody, Clone 2H9 (CBP8595) Monoclonal Antagonist
NRZP-1022-ZP3505 NeuroMab™ Anti-ApoC3 BBB Shuttle Antibody, Clone 14C7 Monoclonal WB; ELISA; Inhib; In Vitro; In Vivo; Antagonist
NRZP-1022-ZP3503 NeuroMab™ Anti-ApoC3 BBB Shuttle Antibody, Clone 5E5 Monoclonal WB; ELISA; Inhib; In Vitro; In Vivo; Antagonist
NRZP-0822-ZP4740 NeuroMab™ Anti-F-Spondin/SPON1 Antibody, Clone N24875P (CBP11839) Monoclonal ELISA

The Potential of NSCs in Huntington's Disease Treatment

Huntington's disease (HD) is caused by mutations in the gene encoding the Huntington protein, which builds up excessively and is detrimental to neural tissue in the lamina propria.

HD mice treated with NSCs have reduced dyskinesia and enhanced spatial memory. Therefore, transplantation of genetically engineered NSCs overexpressing BDNF is recommended for clinical studies in HD patients.

  • NSCs provide trophic support by increasing BDNF levels in the striatal region of the brain, thereby stimulating endogenous NSC growth.
  • Misfolded Huntington protein aggregates were reduced after NSC transplantation.

The Potential of NSCs in Parkinson's Disease Treatment

Parkinson's disease (PD) is a common neurological disorder affecting older adults. The substantia nigra and striatum contain the majority of the lesions in PD. PD causes a decrease in dopamine (DA) levels, which leads to degeneration of dopaminergic neurons. The use of NSCs appears to be an effective technique for PD drug discovery.

  • NSC transplantation has been shown to ameliorate PD-related motor dysfunction, reduce uncoordinated limb movements, enhance neurogenesis, stimulate neuroblast migration, and enhance motor activity.
  • NSCs differentiate into different types of cells in response to the local microenvironment to repair and replenish damaged nerve cells.

A number of antibodies are important tools commonly used in PD research. You can browse the table below to see a list of our recommended products.

Cat. No Product Name Clonality Applications
NAB201250LS Mouse Anti-Human α-Synuclein Phospho (Tyr39) Monoclonal Antibody (CBP3706) Monoclonal IHC-P; ELISA
NAB-08-PZ079 Rabbit Monoclonal Antibody to Alpha-synuclein (phospho S129) Monoclonal WB; DB; ELISA; IHC-P
NRP-0422-P614 NeuroMab™ Anti-Alpha Synuclein Antibody, Clone Syn-O2 Monoclonal DB; ELISA; FC; IHC; In Vitro
NAB-08-PZ735 NeuroMab™ Rabbit Anti-LRRK2 Monoclonal Antibody (CBP1887) Monoclonal ICC; IF; IHC-P; WB

The Potential of NSCs in Multiple Sclerosis Treatment

Multiple sclerosis (MS) is an autoimmune inflammatory disease that affects the CNS when the immune system attacks its tissues, causing multifocal degenerative changes manifested by demyelination and significant neuronal loss in areas of MS. There have been many clinical trials using NSC transplantation for the treatment of MS.

NSCs can exert trophic support, immunomodulation, and metabolic signaling through paracrine mechanisms and cell-to-cell interactions, and promote neuroprotection and tissue repair by reestablishing functional interactions between neural and glial cells or by awakening endogenous neural cells.

The Potential of NSCs in Spinal Cord Injury Treatment

Spinal Cord Injury (SCI) causes disruption of neuromotor and sensory circuits resulting in permanent damage to neural circuits. There are two pathologic changes associated with spinal cord injury. Destruction of axons and blood vessels is the main pathologic change following spinal cord injury. However, secondary changes such as altered local ion concentrations, uncontrolled blood pressure, decreased spinal cord blood flow, disruption of the blood-brain barrier, activation of the immune response, apoptosis, and excitotoxicity can lead to deterioration of the patient's condition and impair the regenerative process.

Therefore, NSC transplantation therapy may help to inhibit these processes. Clinical data have shown that SCI patients receiving neural transplants have reduced fibrosis and post-injury lesions and increased angiogenesis, oligodendrocyte proliferation, axonal regeneration, and myelin regeneration.


  1. Ottoboni, Linda, Beatrice von Wunster, and Gianvito Martino. "Therapeutic plasticity of neural stem cells." Frontiers in neurology 11 (2020): 516659.
For Research Use Only. Not For Clinical Use.
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