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Updated: Apr 24, 2026

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Assessment of cognition and molecular markers for neuropsychological functions in hypertension
Shruti Tripathi1, Farah Khaliq1, Shiva Narang2
1Department of Physiology, University College of Medical Sciences and GTB Hospital, Delhi, India.
Context:
Hypertension is one of the most common reasons for patients to visit family physicians and disrupts cerebral microcirculation, leading to cognitive decline. While its impact on cognition is known, underlying electrophysiological and molecular mechanisms remain unexplored.
Aim:
This study hypothesizes that assessing molecular markers (NF-κB and Nrf-2) alongside event-related potentials (ERPs) and memory will enhance early detection and intervention, and improve our understanding of hypertension-induced neurocognitive impairment.
Settings And Design:
A total of 30 hypertensive patients (aged 30-59 years, diagnosed for 2-5 years with Grade 1 or 2 hypertension) and 30 age-matched controls were included in this cross-sectional study between May 2023 and November 2024.
Method:
Cognition was assessed using auditory ERP and the Post-Graduate Institute Memory Scale. Molecular markers were evaluated using real-time polymerase chain reaction.
Statistical Analysis:
Unpaired t-test and Mann-Whitney U test were used.
Results:
Hypertensive individuals exhibited prolonged P300 latency (P ≤ 0.05), improved mental balance (P = 0.02), and elevated NF-κB levels (P ≤ 0.05). A positive correlation was observed between NF-κB levels and both P300 latency and mental balance, while a negative correlation was noted between NF-κB and retention of dissimilar pairs.
Conclusions:
Hypertension may impair cognition, shown by prolonged P300 latency and elevated NF-κB levels. Their positive correlation suggests inflammation slows processing. Higher NF-κB linked to better mental balance may reflect adaptation, but its negative correlation with retention of dissimilar pairs with memory retention suggests neuroinflammation adversely affects specific cognitive functions.
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