Background <p>Subjective cognitive decline (SCD) is an early sign of Alzheimer’s disease, in which oxidative stress is implicated. Three primary endogenous antioxidants include superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT). This current study aimed to explore the roles of these antioxidants in cognitive outcome of SCD.</p> Methods <p>Sixty-seven adults with SCD were recruited. Cognitive function (assessed by the Alzheimer’s disease assessment scale-cognitive subscale [ADAS-cog]), global function (by Alzheimer’s Disease Cooperative Study scale for ADL [ADCS-ADL]), and plasma GSH, CAT, and SOD were measured at baseline and two years later.</p> Results <p>Over the two-year course, the 67 participants’ cognitive performance (mean ADAS-cog score: 5.2 ± 3.4 at baseline vs. 6.1 ± 5.2 at endpoint, <i>P</i> = .062) and global function (ADCS-ADL score: 68.5 ± 10.2 vs. 62.5 ± 13.3, <i>P</i> &lt; .001) showed a deteriorating trend. Their GSH levels fell significantly (3.67 ± 2.70 vs. 2.81 ± 2.51&#xa0;μm, <i>P</i> = .016), CAT rose (67.7 ± 23.4 vs. 91.9 ± 35.1 nmol/min/mL, <i>P</i> &lt; .001), but SOD remained pretty constant (0.145 ± 0.053 vs. 0.158 ± 0.068 U/mL). Using generalized estimating equations to assess longitudinal changes in ADAS-Cog, we discovered that baseline ADAS-cog score (<i>P</i> &lt; .001), BMI (<i>P</i> = .009), and baseline SOD×GSH interaction (<i>P</i> = .034) were associated with cognitive outcomes.</p> Conclusions <p>Cognitive decline in people with SCD was influenced by baseline cognitive level, BMI, and the interaction between SOD and GSH, suggesting that antioxidant interplay may play a crucial role in regulating oxidative stress and consequently cognitive aging.</p>

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Superoxide dismutase and glutathione interact to determine cognitive outcome among people with subjective cognitive decline (SCD): a prospective study

  • Chieh-Hsin Lin,
  • Hsien-Yuan Lane

摘要

Background

Subjective cognitive decline (SCD) is an early sign of Alzheimer’s disease, in which oxidative stress is implicated. Three primary endogenous antioxidants include superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT). This current study aimed to explore the roles of these antioxidants in cognitive outcome of SCD.

Methods

Sixty-seven adults with SCD were recruited. Cognitive function (assessed by the Alzheimer’s disease assessment scale-cognitive subscale [ADAS-cog]), global function (by Alzheimer’s Disease Cooperative Study scale for ADL [ADCS-ADL]), and plasma GSH, CAT, and SOD were measured at baseline and two years later.

Results

Over the two-year course, the 67 participants’ cognitive performance (mean ADAS-cog score: 5.2 ± 3.4 at baseline vs. 6.1 ± 5.2 at endpoint, P = .062) and global function (ADCS-ADL score: 68.5 ± 10.2 vs. 62.5 ± 13.3, P < .001) showed a deteriorating trend. Their GSH levels fell significantly (3.67 ± 2.70 vs. 2.81 ± 2.51 μm, P = .016), CAT rose (67.7 ± 23.4 vs. 91.9 ± 35.1 nmol/min/mL, P < .001), but SOD remained pretty constant (0.145 ± 0.053 vs. 0.158 ± 0.068 U/mL). Using generalized estimating equations to assess longitudinal changes in ADAS-Cog, we discovered that baseline ADAS-cog score (P < .001), BMI (P = .009), and baseline SOD×GSH interaction (P = .034) were associated with cognitive outcomes.

Conclusions

Cognitive decline in people with SCD was influenced by baseline cognitive level, BMI, and the interaction between SOD and GSH, suggesting that antioxidant interplay may play a crucial role in regulating oxidative stress and consequently cognitive aging.