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NCT Number: NCT05065450

Amygdala Memory Enhancement

The objective is to understand how amygdala activation affects other medial temporal lobe structures to prioritize long-term memories. The project is relevant to disorders of memory and to disorders involving affect and memory, including traumatic brain injury and post-traumatic stress disorder.

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Key information

About this study

Direct electrical stimulation (DES) of the basolateral complex of the amygdala (BLA) can improve declarative memory, reflecting the role of the BLA in modulating memory processes in medial temporal lobe (MTL) regions as a function of emotional arousal. Thus, DES can reveal mechanisms of BLA-mediated memory enhancement relevant to human mental health and disease. DES of the BLA can be used to interrogate the function of memory circuits, especially how neuronal oscillations in the MTL support declarative memory. First, BLA is hypothesized to wield the capacity to prioritize long-term retention of information initially encountered adjacent in time over days and weeks after encoding. Second, the BLA preferentially projects to anterior MTL regions and thus is hypothesized to preferentially modulate memory processes in those anatomic regions, processes thought to support memory for non-spatial items more so than memory for spatial locations. Third, although emotional arousal, amygdala activity, MTL activity, and memory performance are typically correlated, the investigators hypothesize that DES will reveal that BLA outputs to other MTL regions cause improved memory performance by directly eliciting pro-memory oscillatory states in those networks. The expected outcomes represent a significant advancement for the basic science of normal memory function and significant movement towards novel therapeutics designed to emulate endogenous mechanisms of memory enhancement.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Must be able to understand and speak English.
  • Able to provide informed consent.
  • Diagnosed with epilepsy.
  • Scheduled to undergo long-term intra-cranial video monitoring for seizure onset localization.
  • Must be implanted with intracranial depth electrodes to the left or right amygdala, hippocampus, and parahippocampal/perirhinal cortices.

Exclusion criteria

  • Unable to understand and speak English.
  • Unable to provide informed consent.
  • Not diagnosed with epilepsy.

Treatment and study plan

Intracranial Stimulation

Device

Electrodes localized to the BLA will be stimulated with either active-BLAES (0.5-3.5 mA, theta-modulated gamma burst) electrical stimulation for a 1-sec duration immediately following item image presentation or sham-BLAES (zero-amplitude). At later stages of the project, stimulation parameters and timing will be varied and triggered not at random, but by real-time closed-loop analysis of memory biomarkers in the medial temporal lobe.

Other names: Device: ACTIVE basal lateral amygdala electrical stimulation (Active-BLAES), Device: SHAM basal lateral amygdala electrical stimulation (Sham-BLAES)

Primary outcomes

  1. Free recall memory discriminability index (proportion recalled)

    Time frame: 5 years

    Proportion of items (objects, associations, and scenes) accurately recalled during the delayed recall trial will be compared with and without BLAES for each participant in a within subject design. Subsets of items may be tested after durations up to a month after initial presentation.

  2. Recognition memory discriminability index (proportion recalled)

    Time frame: 5 years

    Proportion of items (objects, associations, and scenes) accurately recognized during the delayed recognition trial will be compared with and without BLAES for each participant in a within subject design. Subsets of items may be tested after durations up to a month after initial presentation.

Secondary outcomes

  1. Location of single pulse evoked potential (SPEP) response to amygdala stimulation

    Time frame: 5 years

    Measured by presence of the evoked potential in different brain subregions (hippocampus, entorhinal cortex, perirhinal cortex, and parahippocampal cortex).

  2. Amplitude of SPEP response to amygdala stimulation

    Time frame: 5 years

    Measured in microvolts.

  3. Latency of SPEP response to amygdala stimulation

    Time frame: 5 years

    Measured in milliseconds.

  4. Local field potential (LFP) of good memory state

    Time frame: 5 years

    Measured by relative power spectral frequency recorded at time of item presentation that predicts accurate subsequent memory performance.

  5. LFP of bad memory state

    Time frame: 5 years

    Measured by relative power spectral frequency recorded at the time of item presentation that predicts inaccurate subsequent memory performance

Study contacts

Contact information is provided by the study sponsor or research team.

Joan Atencio

CONTACT

[email protected]

314-362-3114

Sophie Church

CONTACT

[email protected]

917-699-9097

Sponsors and collaborators

Lead sponsor

Washington University School of Medicine

Other

Registry information

Official study title

Mechanisms of Amygdala-Mediated Memory Enhancement in Humans

Important dates

Study start
2021
Primary completion
2026
Study completion
2027
First posted
Oct 4, 2021
Registry last updated
Jul 17, 2025

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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