Alzheimer disease(AD) [30–32] |
Aβ deposition; Autophagy and metabolic dysfunction; Synapse damage and synaptic dysfunction; Imbalance of divalent cation in vivo; Oxidative stress; Tau protein hyperphosphorylation; Central cholinergic neuron injury and so on. |
Improved the Mg2+ level, and adjusted the permeability of BBB-penetrating peptide and cause Aβ deposition decrease; Induced Ca2+ influx to enhance basal autophagy; Participated in the occurrence of oxidative stress. |
Parkinson’s disease (PD) [20,33–35] |
Substantia nigra dopamine neuron degeneration; Oxidative stress; Genetics;Environmentand so on |
Activated pro-apoptotic signaling pathways and particaipated in neurodegeneration of dopaminergic neurons and terminals. |
Amyotrophic Lateral Sclerosis (ALS) [29,36,37] |
Motor neuron injury; Genetics;Environmentand so on. |
Develop a molecular complex with vesicles and participate in regulating the release of neurotransmitters. |
Stroke [38–41] |
Glutamate receptor-mediated Ca2+ overload and neurotoxicity. |
Key of neuronal injury in ischemic conditions: mediated Ca2+ toxicity, mediate Zn2+ toxicity. |
Multiple sclerosis (MS) [42] |
Inflammatory demyelination of white matter in the central nervous system. |
Regulated the formation of glial scars and led to impaired nerve function. |