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.
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.
Reference
- Ottoboni, Linda, Beatrice von Wunster, and Gianvito Martino. "Therapeutic plasticity of neural stem cells." Frontiers in neurology 11 (2020): 516659.
- NeuroMab™ Anti-EPHB2 Antibody(NRP-0422-P1220) (Cat#: NRP-0422-P1220)
- NeuroMab™ Anti-SEZ6 Antibody(NRP-0422-P517) (Cat#: NRP-0422-P517)
- NeuroMab™ Anti-SEZ6 Antibody(NRP-0422-P515) (Cat#: NRP-0422-P515)
- NeuroMab™ Anti-TREM2 Antibody(NRP-0422-P792) (Cat#: NRP-0422-P792)
- Mouse Anti-Human α-Synuclein Phospho (Tyr39) (CBP3706) (Cat#: NAB201250LS)
- NeuroMab™ Anti-Tau Antibody(NRP-0422-P2293) (Cat#: NRP-0422-P2293)
- NeuroMab™ Anti-Tau Antibody(NRP-0422-P1684) (Cat#: NRP-0422-P1684)
- NeuroMab™ Anti-Tau Antibody(NRP-0422-P1686) (Cat#: NRP-0422-P1686)
- NeuroMab™ Rabbit Anti-Alpha-synuclein (CBP1631) (Cat#: NAB-08-PZ079)
- NeuroMab™ Mouse Anti-EFNB2 Monoclonal Antibody (CBP1159) (Cat#: NAB-0720-Z4396)
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- Human huntingtin (HTT) (NM_002111) ORF clone, Myc-DDK Tagged (Cat#: NEP-0521-R0497)
- Mouse Parkinson disease (autosomal recessive, early onset) 7 (Park7) (NM_020569) clone, Untagged (Cat#: NEP-0621-R0133)
- Human huntingtin-associated protein 1 (HAP1) transcript variant 2 (NM_177977) ORF clone, Myc-DDK Tagged (Cat#: NEP-0521-R0676)
- Lenti of Mouse synuclein, alpha (Snca) transcript variant (NM_001042451) ORF clone, mGFP Tagged (Cat#: NEP-0521-R0864)
- Human superoxide dismutase 1, soluble (SOD1) (NM_000454) ORF clone, TurboGFP Tagged (Cat#: NEP-0521-R0748)
- Lenti of Human TAR DNA binding protein (TARDBP) (NM_007375) ORF clone, mGFP Tagged (Cat#: NEP-0521-R0832)
- Human apolipoprotein E (APOE) (NM_000041) ORF clone, Untagged (Cat#: NEP-0421-R0232)
- Human presenilin 1 (PSEN1), transcript variant 2 (NM_007318) ORF clone, TurboGFP Tagged (Cat#: NEP-0421-R0140)
- Tau Antisense Oligonucleotide (IONIS-MAPTRx) (Cat#: NV-2106-P29)
- NeuroBiologics™ Monkey Cerebrospinal Fluid (Cat#: NRZP-0822-ZP495)
- NeuroBiologics™ Pig Cerebrospinal Fluid (Cat#: NRZP-0822-ZP498)
- NeuroBiologics™ Human Cerebrospinal Fluid (Cat#: NRZP-0822-ZP491)
- NeuroBiologics™ Mouse Cerebrospinal Fluid (Cat#: NRZP-0822-ZP497)
- NeuroBiologics™ Rat Cerebrospinal Fluid (Cat#: NRZP-0822-ZP496)
- NeuroPro™ Anti-IDUA BBB Shuttle Protein (Cat#: NRZP-0423-ZP498)
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