Preclinical studies of human platelet lysate and extracellular vesicle preparations for the treatment of neurological diseases
Material . | Disease . | Platelet preparation, model, and administration route . | Biological effects . | References . |
---|---|---|---|---|
HPL | Stroke | PMCAO Intracerebroventricular | NSC proliferation and angiogenesis Improved cognition | 49 |
AD | Primary cortical and hippocampal neurons APP/PS1 mouse model; intranasal delivery | Proliferation and survival of primary neurons Hippocampal neurogenesis and reduced Aβ-induced neurodegeneration | 121 | |
PD | Human dopaminergic neuroblastoma cell line (SH-SY5Y) treated with MPP+MPTP mouse model; intranasal administration | Protection against MPP+ toxicity Diminished inflammatory responses Improved motor performance | 122 | |
LUHMES cells exposed to MPP+MPTP mouse model; intranasal administration | In vitro and in vivo protection of dopaminergic neurons | 119 | ||
LUHMES cells exposed to prooxidants and regulated cell death inducers | Strong neuroprotection through activation of the Akt and MEK pathways | 123 | ||
LUHMES cells; primary cortical and hippocampal neurons | Enhanced expression of tyrosine hydroxylase and neuron-specific enolase in LUHMES cells and strong protection against ferroptosis | 117 | ||
BI and TBI | Proliferating SEZ-derived NPCs | Increased proliferating SEZ-derived NPCs maintaining proliferative or lineage-differentiation capacity | 46 | |
Undifferentiated SH-SY5Y neuroblastoma cells; Ea-hy926 human endothelial cell; BV2 microglial cells | No toxicity and no inflammation Stimulation of wound healing and neuronal differentiation of SH-SY5Y | 125 | ||
Scratch assay (differentiated SH-SY5Y cells) Mouse models of TBI; topical followed by daily intranasal administration | Wound healing Improved motor function; mitigation of cortical neuroinflammation and oxidative stress in the injured area; reduced loss of cortical synaptic proteins | 40 | ||
ALS | NSC34 motoneurons exposed to various neurotoxins | Strong neuroprotection through activation of the Akt and MEK pathways | 123 | |
Motoneuron cultures SOD1G86R; intracerebroventricular or intranasal administration | Akt-dependent neuroprotection, antiapoptotic and antiferroptotic actions Increased lifespan | 126 | ||
EVs | Stroke | PMCAO in vivo model; topical application by biodegradable polymer | Neurogenesis and angiogenesis Improved behavioral function | 48 |
BI and TBI | In vitro assay of NSC proliferation, survival, and differentiation | Increased proliferation, survival, and differentiation, through ERK and Akt signaling | 47 | |
Wound healing (SH-SY5Y) Mouse primary neuronal cells | Nontoxicity Promotion of cell growth and migration Stimulation of network formation in primary neuronal cultures | 130 |
Material . | Disease . | Platelet preparation, model, and administration route . | Biological effects . | References . |
---|---|---|---|---|
HPL | Stroke | PMCAO Intracerebroventricular | NSC proliferation and angiogenesis Improved cognition | 49 |
AD | Primary cortical and hippocampal neurons APP/PS1 mouse model; intranasal delivery | Proliferation and survival of primary neurons Hippocampal neurogenesis and reduced Aβ-induced neurodegeneration | 121 | |
PD | Human dopaminergic neuroblastoma cell line (SH-SY5Y) treated with MPP+MPTP mouse model; intranasal administration | Protection against MPP+ toxicity Diminished inflammatory responses Improved motor performance | 122 | |
LUHMES cells exposed to MPP+MPTP mouse model; intranasal administration | In vitro and in vivo protection of dopaminergic neurons | 119 | ||
LUHMES cells exposed to prooxidants and regulated cell death inducers | Strong neuroprotection through activation of the Akt and MEK pathways | 123 | ||
LUHMES cells; primary cortical and hippocampal neurons | Enhanced expression of tyrosine hydroxylase and neuron-specific enolase in LUHMES cells and strong protection against ferroptosis | 117 | ||
BI and TBI | Proliferating SEZ-derived NPCs | Increased proliferating SEZ-derived NPCs maintaining proliferative or lineage-differentiation capacity | 46 | |
Undifferentiated SH-SY5Y neuroblastoma cells; Ea-hy926 human endothelial cell; BV2 microglial cells | No toxicity and no inflammation Stimulation of wound healing and neuronal differentiation of SH-SY5Y | 125 | ||
Scratch assay (differentiated SH-SY5Y cells) Mouse models of TBI; topical followed by daily intranasal administration | Wound healing Improved motor function; mitigation of cortical neuroinflammation and oxidative stress in the injured area; reduced loss of cortical synaptic proteins | 40 | ||
ALS | NSC34 motoneurons exposed to various neurotoxins | Strong neuroprotection through activation of the Akt and MEK pathways | 123 | |
Motoneuron cultures SOD1G86R; intracerebroventricular or intranasal administration | Akt-dependent neuroprotection, antiapoptotic and antiferroptotic actions Increased lifespan | 126 | ||
EVs | Stroke | PMCAO in vivo model; topical application by biodegradable polymer | Neurogenesis and angiogenesis Improved behavioral function | 48 |
BI and TBI | In vitro assay of NSC proliferation, survival, and differentiation | Increased proliferation, survival, and differentiation, through ERK and Akt signaling | 47 | |
Wound healing (SH-SY5Y) Mouse primary neuronal cells | Nontoxicity Promotion of cell growth and migration Stimulation of network formation in primary neuronal cultures | 130 |
BI, brain injury; NSC, neural stem cell; PMCAO, permanent distal middle cerebral artery occlusion; SEZ, subependymal zone.