Is dorsolateral prefrontal cortex plasticity impaired in Alzheimer disease? Yes, according to researchers writing in JAMA Psychiatry. Dorsolateral prefrontal cortex plasticity is impaired in Alzheimer disease and is associated with impaired working memory.
Findings: In this cross-sectional study of 32 participants with early Alzheimer disease and 16 healthy control participants, significant deficits in dorsolateral prefrontal cortex plasticity were found in participants with Alzheimer disease compared with controls. Working memory performance was also significantly impaired in participants with Alzheimer disease and was associated with dorsolateral prefrontal cortex plasticity across both groups.
Main Outcomes and Measures: Plasticity of the DLPFC measured as potentiation of cortical-evoked activity using paired associative stimulation (a combination of peripheral nerve electrical stimulation and transcranial magnetic stimulation) combined with electroencephalography. Working memory was assessed with the n-back task (1- and 2-back) and measured using the A’ statistic.
Results: Among the 32 participants with AD, 17 were women and 15 were men (mean [SD] age, 76.3 [6.3] years); among the 16 controls, 8 were men and 8 were women (mean [SD] age, 76.4 [5.1] years). Participants with AD had impaired DLPFC plasticity (mean [SD] potentiation, 1.18 [0.25]) compared with controls (mean [SD] potentiation, 1.40 [0.35]; F1,44 = 5.90; P = .02; between-group comparison, Cohen d = 0.77; P = .01). Participants with AD also had impaired performances on the 1-back condition (mean [SD] A′ = 0.47 [0.30]) compared with controls (mean [SD] A′ = 0.96 [0.01]; Cohen d = 1.86; P < .001), with similar findings for participants with AD on the 2-back condition (mean [SD] A’ = 0.29 [0.2]) compared with controls (mean [SD], A′ = 0.85 [0.18]; Cohen d = 2.83; P < .001). Plasticity of DLPFC was positively associated with working memory performance on the 1-back A′ (parameter estimate B [SE] = 0.32 [0.13]; standardized β = 0.29; P = .02) and 2-back A′ (B [SE] = 0.43 [0.15]; β = 0.39; P = .006) across both groups after controlling for age, education, and attention.
Conclusions and Relevance: This study demonstrated impaired in vivo DLPFC plasticity in patients with AD. The findings support the use of DLPFC plasticity as a measure of DLPFC function and a potential treatment target to enhance DLPFC function and working memory in patients with AD.
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