ABSTRACT
Growing evidence demonstrates that meditation practice supports cognitive functions including attention and interoceptive processing, and is associated with structural changes across cortical networks including prefrontal regions, and the insula. However, the extent of subcortical morphometric changes linked to meditation practice is less appreciated. A noteworthy candidate is the Pineal Gland, a key producer of melatonin, which regulates circadian rhythms that augment sleep-wake patterns, and may also provide neuroprotective benefits to offset cognitive decline. Increased melatonin levels as well as increased fMRI BOLD signal in the Pineal Gland has been observed in mediators vs. controls. However, it is not known if long-term meditators exhibit structural change in the Pineal Gland linked to lifetime duration of practice. In the current study we performed Voxel-based morphometry (VBM) analysis to investigate: 1) whether long-term meditators (LTMs) (n=14) exhibited greater Pineal Gland integrity compared to a control group (n=969), 2) a potential association between the estimated lifetime hours of meditation (ELHOM) and Pineal Gland integrity, and 3) whether LTMs show greater Grey Matter (GM) maintenance (BrainPAD) that is associated with Pineal Gland integrity. The results revealed greater Pineal Gland integrity and lower BrainPAD scores (younger brain age) in LTMs compared to controls. Exploratory analysis revealed a positive association between ELHOM and greater signal intensity in the Pineal Gland but not with GM maintenance as measured by BrainPAD score. However, greater Pineal integrity and lower BrainPAD scores were correlated in LTMs. The potential mechanisms by which meditation influences Pineal Gland function, hormonal metabolism, and GM maintenance are discussed - in particular melatonin's roles in sleep, immune response, inflammation modulation, and stem cell and neural regeneration.
ABSTRACT
Physical activity (PA) is a key component for brain health and Reserve, and it is among the main dementia protective factors. However, the neurobiological mechanisms underpinning Reserve are not fully understood. In this regard, a noradrenergic (NA) theory of cognitive reserve (Robertson, 2013) has proposed that the upregulation of NA system might be a key factor for building reserve and resilience to neurodegeneration because of the neuroprotective role of NA across the brain. PA elicits an enhanced catecholamine response, in particular for NA. By increasing physical commitment, a greater amount of NA is synthetised in response to higher oxygen demand. More physically trained individuals show greater capabilities to carry oxygen resulting in greater Vo2max - a measure of oxygen uptake and physical fitness (PF). In the current study, we hypothesised that greater Vo2 max would be related to greater Locus Coeruleus (LC) MRI signal intensity. As hypothesised, greater Vo2max related to greater LC signal intensity across 41 healthy adults (age range 60-72). As a control procedure, in which these analyses were repeated for the other neuromodulators' seeds (for Serotonin, Dopamine and Acetylcholine), weaker associations emerged. This newly established link between Vo2max and LC-NA system offers further understanding of the neurobiology underpinning Reserve in relationship to PA. While this study supports Robertson's theory proposing the upregulation of the noradrenergic system as a possible key factor building Reserve, it also provide grounds for increasing LC-NA system resilience to neurodegeneration via Vo2max enhancement.
