Skip to main content

Table 2 miRNAs associated with Alzheimer’s disease

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.

[42, 150, 159, 160]

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.

[150, 162, 163]

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.

[158, 164]

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.

[165, 166]

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.

[161, 165, 167]

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.

[168,169,170]

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.

[168, 171]

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.

[154, 172, 173]

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.

[156, 174]

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.

[156, 175, 176]

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.

[177,178,179]

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.

[180, 181]

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.

[148, 182, 183]

miR-103

Blood plasma

Expression of miR-103 is decreased in the blood plasma of AD patients.

[148, 151, 158, 184]

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.

[151, 158, 164, 185]

  1. APP, amyloid precursor protein; BACE1, beta-site amyloid precursor protein cleaving enzyme 1; BDNF, brain-derived neurotrophic factor; CDK5, cyclin-dependent kinase 5; CSF, cerebrospinal fluid; MCI, mild cognitive impairment; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; TNF, tumor necrosis factor