Publications by authors named "S Camandola"
Biological clocks and other molecular biomarkers of aging are difficult to implement widely in a clinical setting. In this study, we used routinely collected hematological markers to develop an aging clock to predict blood age and determine whether the difference between predicted age and chronologic age (aging gap) is associated with advanced aging in mice. Data from 2,562 mice of both sexes and three strains were drawn from two longitudinal studies of aging.
View Article and Find Full Text PDFIntroduction: Transcranial Magnetic Stimulation (TMS) is a noninvasive technique that uses pulsed magnetic fields to affect the physiology of the brain and central nervous system. Repetitive TMS (rTMS) has been used to study and treat several neurological conditions, but its complex molecular basis is largely unexplored.
Methods: Utilizing three experimental rat models (, , and ) and employing genome-wide microarray analysis, our study reveals the extensive impact of rTMS treatment on gene expression patterns.
Article Synopsis
- The choroid plexus (CP) produces insulin, which influences food intake and anxiety levels in the brain through signaling pathways.
- Increasing insulin in CP reduces food consumption and anxiety, while reducing insulin has the opposite effects, indicating its significant role in regulating these behaviors.
- Changes in brain gene expression related to synapse activity were observed along with direct effects of CP-derived insulin on the hypothalamus, highlighting the CP's importance in brain insulin signaling.
Article Synopsis
- * A study placed 14-month-old female mice on various dietary plans, focusing on how CR and TRF with different eating windows affect their health, disease progression, and lifespan.
- * Results indicated that CR led to more significant health benefits, unique serum profiles, and increased lifespan compared to TRF, suggesting that prolonged fasting combined with lower energy intake offers better advantages, especially in older female mice.
Article Synopsis
- Alzheimer's disease (AD) is linked to the aggregation of amyloid-β peptide (Aβ1-42), and the FAD-deficient form of NQO1 (NQO1*2) appears to accelerate this process compared to the wild-type form.
- Experiments showed that Aβ1-42 aggregates faster in the presence of NQO1*2, which is unable to bind FAD, and a specific inhibitor can slow down this aggregation.
- The study found that Aβ1-42 and NQO1 isoforms coaggregate into larger structures, providing insights into the mechanisms of amyloid aggregation that may have implications for understanding and treating amyloid-related diseases.