Overview
Overview
Parent Cell: Akira Neural Stem Cells (NSC) differentiated from UCT-WJ-MSCs | Neurotrophic factor-rich exosomes capable of crossing the blood-brain barrier; targeting neurodegeneration, TBI, stroke, and cognitive decline
FOR RESEARCH USE AND INTERNATIONAL USE ONLY
| Source & Manufacturing |
|---|
| 110 Billion Exosomes / 1 mL vial |
| Neurotrophic factor enrichment (BDNF, GDNF confirmed by ELISA 200 pg/mL per vial) |
| miR-124 / miR-132 confirmed by qPCR |
| NTA mean size 85–110 nm |
| Stored at 80°C. |
Definition
What Are Exosomes?
Exosomes are nanoscale extracellular vesicles (40–150 nm) formed by inward budding of endosomal multivesicular bodies (MVBs) and released upon MVB fusion with the plasma membrane. They carry a protected cargo of mRNAs, miRNAs, proteins, lipids, and signaling molecules from their parent cell, delivering this molecular payload to recipient cells with high specificity and efficiency. Unlike the parent cell, exosomes carry no nuclear material and cannot self-replicate — providing a cell-free therapeutic profile with superior safety and stability characteristics.
Process
Mechanism of Action & Molecular Cargo
Blood-Brain Barrier Penetration: Neural exosomes' phospholipid membrane with Lamp2b targeting enables trans-BBB delivery, concentrating neurotrophic cargo directly in CNS tissue after IV or intranasal administration.
Neurogenesis Promotion: BDNF and GDNF protein mRNA cargo activates TrkB and GFRα1 receptors on neurons, stimulating axonal growth, synaptic potentiation (LTP), and hippocampal neurogenesis — directly relevant in Alzheimer's and cognitive decline.
Neuroinflammation Suppression: miR-124 suppresses microglial M1 activation by targeting C/EBPα and STAT3, shifting microglia toward M2 neuroprotective phenotype. miR-132 targets acetylcholinesterase, improving cholinergic signaling in AD.
Axonal Repair & Remyelination: miR-21 and NT-3 cargo supports oligodendrocyte precursor survival and differentiation, promoting remyelination in MS and spinal cord injury models.
Apoptosis Prevention: Anti-apoptotic Bcl-2 family mRNA and miRNAs (miR-21, miR-let7) prevent ischemia-induced neuronal death in the penumbra zone post-stroke.
Biomarkers
Key Molecular Cargo
| Molecule / miRNA | Therapeutic Function |
|---|---|
| BDNF / GDNF / NGF protein | Neurotrophic factors; neuronal survival, synaptic plasticity |
| miR-124 | Microglial M1 suppression; neuroinflammation resolution |
| miR-132 | Acetylcholinesterase suppression; memory and cognitive improvement |
| miR-21 | Neuronal anti-apoptosis; PTEN/PI3K/Akt activation |
| NT-3 / CNTF | Oligodendrocyte support; remyelination promotion |
| VEGF mRNA | Stroke recovery; angiogenesis in ischemic brain tissue |
| Synapsin-1 / PSD-95 mRNA | Synaptic protein cargo; synaptic remodeling support |
Applications
Therapeutic Applications
- Alzheimer's Disease — BDNF/miR-132 delivery, amyloid burden reduction
- Parkinson's Disease — GDNF neuroprotection, dopaminergic support
- Traumatic Brain Injury (TBI) — BBB repair, neuroinflammation resolution
- Stroke Recovery — penumbra rescue, neurogenesis, angiogenesis
- Multiple Sclerosis — remyelination support, neuroinflammation suppression
- Spinal Cord Injury — axonal regeneration signals
- ALS — motor neuron survival extension
- Cognitive Decline & Dementia
- Autism Spectrum Disorder — neuroinflammation, GABA/glutamate balance
- Depression — hippocampal neurogenesis via BDNF delivery
Evidence
Clinical & Preclinical Evidence
A 2023 review in Bioengineering (PMC9952071) covering 88 publications on MSC and NSC exosomes in Alzheimer's disease confirmed: miR-132 delivery reduces tau phosphorylation, BDNF delivery preserves hippocampal neurons, and NSC exosomes cross the BBB effectively. Multiple preparations reduced Aβ plaque burden and improved Morris water maze performance in AD mouse models.[1]
UC-MSC-derived exosomes attenuated LPS-induced neuroinflammation in vivo through the NRF2/NF-κB/NLRP3 pathway — reducing IL-1β, IL-18, TNF-α, and reactive oxygen species in brain tissue. This mechanism is directly reproduced and amplified in neural-lineage-specific exosomes.[2]
In TBI models, IV-administered UC-MSC exosomes (100 μg protein equivalent) reduced lesion volume by 35%, improved neurological severity scores by 42%, and enhanced hippocampal BDNF levels 3× vs control at 7 days post-injury — establishing efficacy in acute neurological trauma.
In stroke (MCAO) models, intranasal delivery of neural exosomes activated endogenous neurogenesis (BrdU+/DCX+ cells), increased angiogenesis in the ischemic penumbra (CD31+ vessel density), and improved functional outcomes (Garcia score) at 14 days — supporting intranasal as a clinical delivery route.[3]