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Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions

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A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.

Wan-Rong Jiang^1,2, Yong-Ming Zhou¹, Wei Wu³

¹Department of Geriatrics, Renmin Hospital of Wuhan University, Wuhan, China.

|January 17, 2024

Summary

Chronic Cerebral Hypoperfusion (CCH) causes cognitive dysfunction by damaging neuronal fibers and increasing neuroinflammation. Circular RNAs (circRNAs) play a key role, offering potential therapeutic targets for CCH.

Keywords:

RNA sequencing ceRNA chronic cerebral hypoperfusion cognitive dysfunction

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Area of Science:

Neuroscience
Molecular Biology
Pathology

Background:

Chronic Cerebral Hypoperfusion (CCH) is linked to cognitive decline, but its mechanisms are not fully understood.
Existing knowledge gaps hinder the development of effective treatments for CCH-induced cognitive dysfunction.

Purpose of the Study:

To investigate the neuropathological mechanisms underlying CCH.
To explore the role of messenger RNAs (mRNAs) and circular RNAs (circRNAs) in CCH.
To identify potential therapeutic targets for CCH.

Main Methods:

Utilized an established animal model of Chronic Cerebral Hypoperfusion (CCH).
Assessed neuropathological changes including neuronal fiber integrity (MAP2, MBP staining), neuroinflammation (astrocyte/microglia markers), and synaptic loss.
Performed RNA sequencing to analyze differential expression of mRNAs and circRNAs, followed by GO and KEGG pathway analyses.
Constructed a circRNA-miRNA-mRNA competing endogenous RNA (ceRNA) network.

Main Results:

CCH led to reduced neuronal fibers and demyelination, without altering neuron count.
Increased neuroinflammation, glial cell activation, and synaptic loss were observed in CCH.
RNA sequencing revealed significant alterations in mRNA and circRNA expression, enriched in immune and inflammatory pathways.
The ceRNA network highlighted the role of neuroinflammation and highlighted DE circRNAs co-expressing with DE mRNAs.

Conclusions:

CCH induces significant neuropathological changes, including neuronal fiber damage and neuroinflammation.
circRNAs are implicated in CCH pathogenesis and may serve as crucial regulators of neuroinflammatory responses.
circRNAs represent promising therapeutic targets for mitigating CCH-related cognitive dysfunction.