Mechanism of Gamma Oscillation Synchronization in the Prefrontal-hippocampal Circuit for Memory Dysfunction in Patients With White Matter Lesions of Cerebral Small Vessel Disease

Trial statusRecruiting
Trial phaseNot listed
Trial typeObservational
Biological sexAll
Age55-75
SponsorXuanwu Hospital, Beijing

About this trial

The mechanism underlying memory impairment caused by white matter lesions of cerebral small vessel disease is still unclear. The disrupted synchronization of gamma oscillations in the prefrontal-hippocampal circuit is a potential key mechanism. Our study has demonstrated that white matter lesions lead to demyelination of the connection tracts between the prefrontal lobe and hippocampus, which is closely related to memory dysfunction. However, further studies are required to explore if these microstructural changes in white matter tracts influence memory function by affecting gamma oscillations. Thus, this project will use the previously established episodic memory task and event-related potential to determine the changes in gamma oscillations in the prefrontal-hippocampal circuit and the effects on memory encoding and retrieval. Combining multimodal imaging, we will explore the mediating role of white matter microstructure damage, and establish a machine learning prediction model for memory impairment. In addition, transcranial alternation current stimulation (tACS) will be used to investigate the mechanisms of memory improvement by regulating the prefrontal-hippocampal gamma oscillations. This project will clarify the neural oscillation mechanism underlying memory impairment caused by white matter lesions of cerebral small vessel disease, with the expectation of providing new predictive indicators and interventions.

Eligibility criteria

This trial accepts healthy volunteers

Qualifiers

- Individuals with cerebral small vessel disease, normal cognition or mild cognitive impairment subjects;

Participants with complete demographic data, neuropsychiatric scale assessments, imaging data, and EEG data.

Disqualifiers

Severe aphasia, physical disability, or other conditions preventing completion of neuropsychological assessments;

History of cerebrovascular stroke with documented neurological deficits during onset and corresponding lesions on neuroimaging;

Neurological disorders that may cause cognitive impairment, including alcohol abuse, drug addiction, traumatic brain injury, epilepsy, encephalitis, or normal-pressure hydrocephalus;

Systemic diseases potentially contributing to mild cognitive impairment (e.g., hepatic/renal insufficiency, endocrine disorders, vitamin deficiencies);

Trial population

Elderly population

Trial design

Design model

Cohort

Time perspective

Prospective

Treatments tested in this trial

Not listed

Trial groups

No trial groups listed

Trial outcomes

Primary outcomes

1

Overall cognitive function

Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MOCA) scale scores.

Time frame
baseline and one-year follow-up

Secondary outcomes

1

Attention and executive functions

the scores are evaluated using the Clock Drawing Test (CDT), the Digit Span Test (DST), and the Trail Making Test (TMT).

Time frame
Baseline and follow up
2

Language function

Boston Naming Test (BNT)

Time frame
Baseline and one-year follow up
3

Memory function

Digit Span Test (DST) and the WHO-UCLA Auditory Verbal Learning Test (AVLT).

Time frame
Baseline and one-year follow up
4

Brain imaging data

Based on DTI data, the following metrics can be extracted: Fractional Anisotropy (FA) Mean Diffusivity (MD) Axial Diffusivity (AD) Radial Diffusivity (RD)

Time frame
baseline and one-year follow-up

Other outcomes

Sponsors and contacts

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