Table 1.
The roles of MIF in AD.
| Authors | Study design | Results |
|---|---|---|
| Popp et al. 2009 [25] | AD patients: mean age (years) = 69.77, gender (m/f) = 12/19 MCI patients: mean age (years) = 67.04, gender (m/f) = 20/8 Control: mean age (years) = 67.05, gender (m/f) = 12/7 |
CSF MIF increased positively with TNF-α production. |
| Bacher et al.2010 [26] | AD patients: mean age (years) = 66.71, gender (m/f) = 5/2 Control: mean age (years) = 66.57, gender (m/f) = 5/2 APP 23 transgenic mouse |
CSF MIF increased. MIF in microglial cells was associated with Aβ plaques. ISO-1 inhibited Aβ-induced neurotoxic in SHSY and BV-2 cells. |
| Zhang et al. 2019 [17] | AD patients: mean age (years) = 69.4, gender (m/f) = 14/14 MCI patients: mean age (years) = 68.9, gender (m/f) = 4/6 Control: mean age (years) = 61.2, gender (m/f) = 14/16 AD patients brain: mean age (years) = 68.4, gender (m/f) = 3/2 Control brain: mean age (years) = 48.4, gender (m/f) = 4/1 APP23/MIF+/− mice |
MIF served as a defense mechanism and a biomarker of AD. MIF upregulated both in CSF and brain tissue. MIF deficiency affected cognitive functions in AD mice. MIF colocalized and interacted with Aβ oligomers. MIF overexpression inhibited Aβ-induced cytotoxicity. |
| Oikonomidi et al. 2017 [32] | CI: mean age (years) = 74.16, gender (m/f) = 44/53 Control: mean age (years) = 66.38, gender (m/f) = 16/36 |
CSF MIF levels were higher in CI with AD which associated with higher CSF tau and p-tau and lower CSF Aβ1–42, independently predicted cognitive decline. |
| Nasiri et al. 2020 [27] | AD patients: mean age (years) = 69.7, gender(m/f) = 10/9 Control: mean age (years) = 70.5, gender (m/f) = 5/9 6-month-old male C57BL/6 or MIF-KO mice subjected to ICV-STZ |
CSF MIF increased and positively associated with tau, p-tau and negative associated with Aβ1–42. ISO-1 improved the STZ-induced memory impairment in contextual by reducing cytokine production. |
| Flex et al. 2014 [34] | AD patients: mean age (years) = 76.6, gender (m/f) = 188/353 Control: mean age (years) = 76.7, gender (m/f) = 268/445 |
No significant difference in the distribution of the CRP, MIF, and TNF-gene polymorphism. |
| Carlred et al. 2016 [29] | 18-month-old transgenic mice (3 male, 1 female) with the Arctic (E693G) and Swedish (K670N, M671L) mutations (tgArcSwe) of human APP | MIF colocalized with activated microglia (Iba1) to the Aβ positive deposits in the hippocampal region. |
| Li et al. 2015 [30] | APP/PS1 transgenic mice were mated with MIF−/− mice 3-6-month-old female WT and MIF−/− mice subjected to ICV-STZ Primary astrocyte were treated with high glucose to mimic STZ function |
ICV-STZ increased astrocyte activation and MIF expression in the hippocampus. MIF deficiency or ISO-1 attenuated tau hyperphosphorylation and astrocyte activation. |
| Liang et al. 2018 [31] | 4-week-old male mice received D-galactose- and AICI3 for 90 d to induced AD model, then administrated Fufang Danshen for 14 d. SH-SY5Y cells |
Fufang Danshen suppressed MIF induced apoptosis in SH-SY5Y cells by decreasing Bad levels via Akt and IKKα/β signals. Fufang Danshen downregulated the levels of MIF, Bad and INF-γ in AD mouse model. |