From: Advances in the development of new biomarkers for Alzheimer’s disease
miRNA | Sample | Project conclusions | References |
---|---|---|---|
miR-125b | Serum, blood, CSF, blood plasma | Level of miR-125b is decreased in the serum of AD group compared to the control group. MiR-125b is upregulated in the AD brain, where it leads to the increased cyclin-dependent kinase 5 expression and tau hyperphosphorylation. MiR-125b downregulates the cell cycle inhibitor CDKN2, and increases proliferation of glial cells. | |
miR-181c | Serum | Level of miR-181c is decreased in the blood of AD and MCI group compared to control group. MiR-181 participates in the fine-tuning of inflammatory processes in astrocytes, decreasing the production of TNF-α, IL-6, IL-1β and IL-8. | |
miR-26b | Serum, blood, CSF | Expression of miR-26b is downregulated in the serum compared to non-inflammatory neurological controls. MiR-26b induces proliferation of postmitotic neurons via targeting Rb tumor suppressor mRNA, which leads to activation of CDK5 kinase involved in Tau phosphorylation and apoptotic neuron death. | |
miR-31 | Serum | Level of miR-31 is decreased in the serum of AD group compared to control group. MiR-31 is downregulated in the brains of AD patients and AD mice. Overexpression of miR-31 reduces amyloid β in hippocampus of transgenic mice through direct targeting of APP and BACE1 mRNAs. | |
miR-146a | Serum | Level of miR-146a is decreased in the serum of AD group compared to control group. MiR-146a is connected to neuroinflammation, and is upregulated by NF-κB, a pro-inflammatory transcription factor. MiR-146a inhibits LRP2 mRNA translation, which also leads to cell apoptosis. | |
miR-29c-3p | Serum | Level of miR-29c-3p is decreased in the serum of AD group compared to control group. MiR-29b-3p targets the BACE1 mRNA. BACE1, also known as beta-secretase 1, promotes the formation of Aβ-plaques by producing Aβ peptides. | |
miR-19b-3p | Serum | Level of miR-19b-3p is decreased in the serum of AD group compared to the control group. MiR-19 inhibits the aluminum-induced apoptosis of neurons. | |
miR-34a-5p | Blood plasma | Expression of miR-34a-5p is downregulated in the serum of AD group compared to control group. The expression of miR-34a is downregulated in response to Aβ, which leads to increased level of its target cyclin-D1 and cell cycle-related apoptosis. | |
miR-206 | Serum | Level of miR-206 is increased in the serum of the MCI group compared to the control group. MiR-206 promotes cognitive decline by suppressing BDNF expression in the brain. | |
miR-132 | Serum | Level of miR-132 is increased in the serum of the MCI group compared to the control group. MiR-132 expression reduces the expression of nitric oxide synthase and oxidative stress in brain tissues via the p38 signaling pathway in a rat AD model. | |
miR-34c | Blood | Level of miR-34c is increased in the blood of AD and MCI groups compared to the control group. Increased miR-34c expression in hippocampal neurons in AD negatively regulates the density of the hippocampal dendritic spine. | |
miR-15b-5p | Blood plasma | Level of miR-15b-5p is decreased in the blood plasma of AD group compared to the control group. MiR-15b-5p targets the amyloid precursor protein mRNA and has a neuroprotective effect. | |
miR-222 | Serum | Expression of miR-222 is decreased in serum in the mild and moderate AD patients compared to the control group. Reduced expression of miR-222 in AD may contribute to cell cycle disruption by altering the expression of cyclin-dependent kinase inhibitor 1B. | |
miR-103 | Blood plasma | Expression of miR-103 is decreased in the blood plasma of AD patients. | |
miR-107 | Blood plasma | Expression of miR-107 is decreased in blood plasma of AD and PD patients compared to the control group. MiR-107 targets the 3’-UTR of BACE1 mRNA. Decreased expression of miR-107 increases the BACE1 protein level, which is responsible for the formation of toxic forms of Aβ. |