Related Experiment Video
Updated: Jul 16, 2026
06:48
Lexical Decision Task for Studying Written Word Recognition in Adults with and without Dementia or Mild Cognitive Impairment
Published on: June 25, 2019
Cortisol awakening response and Val66Met BDNF polymorphism interact to shape verbal fluency in aging
Pablo Rivas-Diaz1, David Trillo-Figueroa1, Teresa Peiró2
1Laboratorio de Neurociencia Social Cognitiva, Departamento de Psicobiología, Universitat de València, Spain.
Psychoneuroendocrinology
|July 14, 2026
Summary
Cognitive aging is influenced by genetic and hormonal factors. Brain-Derived Neurotrophic Factor (BDNF) Val66Met polymorphism affects verbal fluency, but only in individuals with specific genetic profiles.
Area of Science:
- Neuroscience
- Cognitive Aging
- Genetics
Background:
- Neural plasticity underpins cognitive function and declines with age, particularly affecting higher-order abilities like verbal fluency (VF).
- Verbal fluency, encompassing phonemic (PVF) and semantic (SVF) subdomains, serves as a sensitive indicator of cognitive aging.
- Neurotrophic (e.g., BDNF) and neuroendocrine (e.g., CAR) mechanisms influence neural plasticity and cognitive performance.
Purpose of the Study:
- To investigate the interaction between the Cortisol Awakening Response (CAR) and the Brain-Derived Neurotrophic Factor (BDNF) Val66Met polymorphism.
- To examine how this interaction affects phonemic verbal fluency (PVF) and semantic verbal fluency (SVF) in healthy older adults.
Main Methods:
- Studied healthy older adults, assessing their Cortisol Awakening Response (CAR) and BDNF Val66Met genotype.
- Measured performance on phonemic verbal fluency (PVF) and semantic verbal fluency (SVF) tasks.
- Utilized statistical analysis to explore moderating effects of the BDNF polymorphism on the CAR-PVF/SVF relationship.
Main Results:
- A significant moderating effect of the BDNF Val66Met polymorphism was observed in the relationship between CAR and PVF.
- Higher CAR was associated with better PVF performance exclusively in participants homozygous for the Val allele.
- No significant associations were found between CAR, BDNF genotype, and SVF performance.
Conclusions:
- Cognitive aging, specifically PVF, is modulated by a complex interplay between genetic (BDNF) and hormonal (CAR) factors.
- The findings underscore the differential impact of genetic variations on cognitive functions influenced by neurotrophic and endocrine pathways.
More Related Videos
10:13Assessment of Age-related Changes in Cognitive Functions Using EmoCogMeter, a Novel Tablet-computer Based Approach
Published on: February 14, 2014
08:08Eye Tracking, Cortisol, and a Sleep vs. Wake Consolidation Delay: Combining Methods to Uncover an Interactive Effect of Sleep and Cortisol on Memory
Published on: June 18, 2014
Related Concept Videos
01:27Language and Cognition
Language serves as a bridge between ideas and communication, influencing how individuals perceive and interact with the world. Psychologists have long debated whether language shapes thought or vice versa. This discussion gained grip with Edward Sapir and Benjamin Lee Whorf in the 1940s, who proposed that language determines thought, a concept known as linguistic determinism. They suggested that the vocabulary and structure of a language influence how its speakers think and perceive reality.
01:30Cognitive Development During Adulthood
Cognitive development continues throughout adulthood, undergoing significant shifts across early, middle, and late stages. Individual transition occurs from adolescent idealism to pragmatic and adaptable thinking in early adulthood. During this period, individuals learn to integrate personal beliefs with the recognition that other perspectives are equally valid. Exposure to the complexities of modern society, diverse experiences, and higher education contribute to this adaptive thought process,...
01:26Aging
Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
01:27Pharmacodynamics in Geriatric Patients: Effects of Age
Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...