62 research outputs found

    Meditation-induced bliss viewed as release from conditioned neural (thought) patterns that block reward signals in the brain pleasure center

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    The nucleus accumbens orchestrates processes related to reward and pleasure, including the addictive consequences of repeated reward (e.g., drug addiction and compulsive gambling) and the accompanying feelings of craving and anhedonia. The neurotransmitters dopamine and endogenous opiates play interactive roles in these processes. They are released by natural rewards (i.e., food, water, sex, money, play, etc.) and are released or mimicked by drugs of abuse. Repeated drug use induces conditioned down-regulation of these neurotransmitters, thus causing painful suppression of everyday pleasure. As with many spiritual traditions, Buddhism provides strong advice against the pursuit of worldly pleasures to attain the ‘‘good life.’’ In contrast, many forms of meditation give rise to an immense and abiding joy. Most of these practices involve ‘‘stilling the mind,’’ whereby all content-laden thought (e.g., fantasies, daydreams, plans) ceases, and the mind enters a state of openness, formlessness, clarity, and bliss. This can be explained by the Buddhist suggestion that almost all of our everyday thoughts are a form of addiction. It follows that if we turn off this internal ‘‘gossip of ego,’’ we will find relief from the biochemical dopamine/opiate down-regulation, which is, perhaps, the perpetual concomitant of our daily rumination

    New insights into the genetic etiology of Alzheimer's disease and related dementias

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    Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele

    Analysis of shared heritability in common disorders of the brain

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    Paroxysmal Cerebral Disorder
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