• BrainMindSoul

     

    Frontiers Alzheimer Mind Memory Soul

    The topics of the above five books appear unrelated, but they are actually interconnected as indicated by arrows. At the center is "Frontiers in Microtubules" which focuses on the role of microtubules in long-range synchronization that generates brain's alpha, theta and gamma waves. "The Origin of Consciousness" presents evidence for the "Alpha Hypothesis" which posits that consciousness emerges from the global synchronization of the alpha waves. At a more fundamental level, the alpha waves may create a gravitational geon, while the theta and gamma waves encode information about environment and memory that can be consciously perceived when the information (carried by gravitational waves) is bound by the gravitational geon.

    Tau, a microtubule-associated protein, is known to play a central role in . CRMP2, another microtubule-associated protein, has emerged as a key player in bipolar disorder. It could also play a crucial role in memory extinction and retrieval, as detailed in "Born to Forget, Die to Remember". The proposed mechanism can explain a near-death phenomena: life review. The gravitational geon created by a healthy brain is part of the "mind" which, at any moment, includes only a tiny fraction of our life experiences. By contrast, the gravitational geon created by a dying brain may be identified as the "

    Unraveling the Mystery of

    แอพ โหลดเกมฟรีทุกเกม

    The hypofunction of NMDA receptors (NMDARs) in schizophrenia could arise from the occlusion of GluN2B-containing NMDARs by the CABT complex, which consists of a CRMP2 monomer, an alpha and a beta tubulin. Tubulin is the canonical binding partner of CRMP2. Binding between GluN2B and CRMP2 has been demonstrated experimentally (See Paper 25 for details).

    A class of hallucinogenic drugs are agonists of 5-HT2A receptors (5-HT2ARs), yet several 5-HT2AR agonists are not hallucinogens. It has been shown that their major difference could lie in the capacity of hallucinogens to induce the Gi/o pathway. Since the Gi/o pathway inhibits protein kinase A (PKA), this finding supports the CABT Hypothesis where PKA plays a key role in preventing NMDAR hypofunction (i.e., CABT occlusion) by (1) phosphorylating GluN2B at Ser-1166, and (2) inhibiting glycogen synthase kinase 3 (GSK-3). The importance of PKA in NMDAR hypofunction is further underscored by the emergence of phosphodiesterase (PDE) as a therapeutic target for schizophrenia. PDE catalyzes the breakdown of cAMP and/or cGMP. Its inhibitors may elevate cAMP level, thereby enhancing PKA activity. (See Paper 26 for details).

    New

    (2019-02-01) The Roles of 5-HT2A Receptors and mGluR2 in Schizophrenia

    (2018-11-25) Memory Extinction: The Role of Dopamine

    (2018-11-07) The CABT Hypothesis of Schizophrenia

    (2018-09-21) Global Synchronization of Alpha Rhythms

    Updates

    (2019-02-13) Neural Correlates of Conscious Level and Content

    (2018-12-10) The Role of CRMP2 in Mossy Fiber Sprouting

    (2018-12-05) Dendritic Filopodia: the "Tags" for the Formation of Enduring Memory

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