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Within the field of neuroimaging, the discovery of a constellation of brain regions silently active when we are “resting” has provided a new view into the elusive effects of meditative practice. This network, called the default mode network (DMN), has been shown by functional neuroimaging to be active when an individual is at rest. Meta-analyses of the fMRI neurocorrelates of meditation have shown that across diverse practices, the most common general effect appears to be modulation of regions within the DMN. The specific practice of mantra meditation is a form of task-positive concentration. These kinds of task-positive activities are regarded by many to be an anti-correlate of DMN activity, thereby in theory, reducing activations within the DMN as concentration on a particular task increases. Yet previous studies on mantra meditation using language tasks as controls have reported only activations, not deactivationswithin the DMN. A study by Berkovich-Ohana showed that word repetition as control task could mask some of the effects of mantra, which may explain why previous studies using language repetition as control task failed to find significant DMN deactivationsduring mantra meditation. To investigate these differences, we analyzed mantra meditation using a finger-tapping control task which required a minimal amount of focused attention, yet enough to reduce blood flow to the major hubs of the DMN and minimally reduce network activity. Using a finger-tapping control thus modifies the research question: Can a brief course of this kind be shown to modulate DMN activations during mantra practice beyondthat of a minimally active/non-language finger-tapping control condition; and if so, can we see a training effect over time? Our results show that over a 2-week period of Kundalini yoga/meditation, participants successfully decreased activations within subregions of the DMN, namely the pregenual anterior cingulate cortex (PACC) and the precuneus, during mantra meditation with trends toward decreased activation in the posterior cingulate cortex (PCC) as well. These decreased activations were significant despite use of a finger-tapping control task known to deactivate these regions, indicating that mantra practice suppresses activation in these DMN regions beyondthe active control task. These results emphasize the importance of the choice of control task and provide insight into the “mantra effect.” Here, we show that training in mantra meditation, like other practices such as focused attention and open monitoring, also has a suppressive effect on activity within the DMN.

The disease-associated prion protein (PrP) forms aggregates which vary in structural conformation yet share an identical primary sequence. These variations in PrP conformation are believed to manifest in prion strains exhibiting distinctly different periods of disease incubation as well as regionally specific aggregate deposition within the brain. The anionic luminescent conjugated polythiophene (LCP), polythiophene acetic acid (PTAA) has previously been used to distinguish PrP deposits associated with distinct mouse adapted strains via distinct fluorescence emission profiles from the dye. Here, we employed PTAA and 3 structurally related chemically defined luminescent conjugated oligothiophenes (LCOs) to stain brain tissue sections from mice inoculated with 2 distinct prion strains. Our results showed that in addition to emission spectra, excitation, and fluorescence lifetime imaging microscopy (FLIM) can fruitfully be assessed for optical distinction of PrP deposits associated with distinct prion strains. Our findings support the theory that alterations in LCP/LCO fluorescence are due to distinct conformational restriction of the thiophene backbone upon interaction with PrP aggregates associated with distinct prion strains. We foresee that LCP and LCO staining in combination with multimodal fluorescence microscopy might aid in detecting structural differences among discrete protein aggregates and in linking protein conformational features with disease phenotypes for a variety of neurodegenerative proteinopathies.