TABLE 2.
Summary of immunomodulatory therapies used to treat acute neurodegenerative diseases in patients and in animal models
| Immunomodulatory therapies | ||||
|---|---|---|---|---|
| Model/condition | Intervention | Outcome | Study | |
| Acute diseases | ||||
| Stroke |
Rat model of cerebral ischemia (tMCAo‐transient middle cerebral artery occlusion). |
Injection with Cop‐1: 200 μg after reperfusion. |
Neuroprotection and neurogenesis through the stimulation of PA: ‐Significant improvement in neurological deficit. ‐Lower percentage of infarct volume ‐Modulation of the CP microenvironment (upregulation of BDNF, IGF‐1, NT‐3 and IL‐10 in the SVZ, SGZ and CC, which correlated with an increase in neurogenesis; downregulation of IL‐17). |
Ibarra (2007)46 ; Cruz (2015)47 ; Cruz (2018)47 |
| Mouse model of tMCAo. | Injection with GA: 3.5 mg/kg of body weight before the induction of stroke. | No protective effect (stroke volume and functional parameters without significant differences) | Kraft (2014)48 | |
| Mouse model of permanent focal cerebral ischemia occlusion (pMCAo) and tMCAo | Injection with GA: 2 mg in 200 μl SS. after cerebral ischemia in the pMCAo group and immediately after reperfusion in the tMCAo group. |
No protective effect (does not reduce infarct volume or improve neurological deficit): ‐significant increase in neurogenesis in pMCAo ‐Reduction in microglial pro‐inflammatory cytokines (TNFα e IL‐1β) in tMCAo. Microglial cells were activated in both models. |
Poittevin 201349 | |
| SCI | Lewis rat. T7 or T9 spinal cord contusion | Passive (107 T cells specific to MBP) or Active (with MBP) immunization | ‐Enhanced motor and cellular recovery | Hauben (2000)10 |
| Sprague‐Dawley rats. T9‐T10 spinal cord contusion | GA immunization: High dose (2 mg/km, 28 days) or low dose (0.5 mg/ml, 28 days) |
‐GA in high doses has deleterious effects. ‐The response to GA in SCI depends on dose and time of administration |
Askarifirouzjaei (2019)50 | |
| Fischer rats and BALB/c mice. T9 spinal cord injury | GA immunization. Rats: 200 µg at the base of the tail. Mice: 150 µg subcutaneous injection. | ‐Nitric oxide (NO) and inducible nitric oxide synthase (iNOS) gene expression reduction at the site of injury | García (2012)51 | |
| TBI |
C57Bl/6J and BALB/c/OLA mice. Closed head injury model. |
Cop‐1 immunization: intramuscular injection of 100 μg. | Neuroprotective effect: reduction in the spread of damage. | Kinips (2003)52 |