Differential Gene Expression in Human Hippocampus With Aging.

A transcriptomic comparison between young and old hippocampal samples revealed differentially expressed genes linked to multiple biological pathways.

• The study performed transcriptomic analysis from hippocampal samples of individuals of different ages.
• Two complementary analyses were completed: a group comparison (young vs. old) and a correlation analysis with chronological age.
• Differentially expressed genes were linked to inflammation and immune system pathways, DNA repair, metabolism, and neural activity.

Correlation analysis identified a subset of 6 genes whose expression was associated with chronological aging in the human hippocampus.

• This subset was identified through a correlation analysis as a complementary approach to the young vs. old group comparison.
• Among the 6 genes, RAD23B was identified as the most significant.
• RAD23B showed a negative correlation of its mRNA expression with age.

RAD23B mRNA and protein expression negatively correlate with age in the human hippocampus.

• RAD23B was identified as the most significant gene among the age-correlated subset.
• Both mRNA and protein expression of RAD23B showed negative correlation with chronological age.
• RAD23B expression was even lower in patients with Alzheimer's disease compared to aged individuals.

RAD23B is expressed predominantly in neurons and astrocytes in the human hippocampus.

• Cell-type-specific expression analysis showed RAD23B was mostly expressed in neurons and astrocytes.
• Studies in human primary cultures were conducted to assess RAD23B function in these cell types.
• RAD23B was found to be required for cell survival and function in these primary culture studies.

RAD23B expression is reduced in patients with Alzheimer's disease compared to aged controls.

• RAD23B expression in Alzheimer's disease patients was even lower than in older adults without the disease.
• This finding suggests RAD23B may serve as a biomarker linking normal aging to neurodegenerative disease.
• The authors identify RAD23B as 'a putative biomarker and regulator of cell aging in the brain.'

Studies in human primary cultures demonstrated that RAD23B is required for cell survival and function in neurons and astrocytes.

• Human primary cultures of neurons and astrocytes were used to investigate RAD23B function.
• Loss of RAD23B was associated with impaired cell survival.
• RAD23B was also required for normal cell function in these hippocampal cell types.