Tuesday, February 15, 2011

Calcium, Mitochondria and Neuroendocrineimmunology

What do Calcium, a "frigid mother", a 'strange' immune system and energy metabolism have in common?

Many of you hear it coming - Schizophrenia.

Such a bizarre neurological disease process that many feel once cracked (or the way to crack it), will lead to the understanding of the underpinnings of obesity, cancer and many autoimmune disorders, let alone segue into a tremendously prodigious time for the understanding & treatment of other neuropsychiatric illnesses.

An 'old' theory of how to cause it, was to have a 'frigid' or unattached mother -- this is now a MOSTLY discredited and almost forgotten hypothesis of a psychoanalytic origin, which still contains a kernel of truth: mitochondria in humans are transmitted via the maternal line.

This leads to the mound of overwhelming (clinical, genomic, theoretical) evidence that seems to point to mitchondrial changes that impair (to varying degrees of 'penetrance') cellular energy metabolism, transcription/protein-folding/protein-degredation, mechanisms of cellular death and aging.

This in turn leads us to (and from) deranged cellular calcium processing and what it does to other cellular mechanisms (including back to the mitochondria) and processes that affect higher-level systems including immune- and endocrine- systems. These in-turn, effect responses to stimuli, sensory processing, the stress response, methyl-pool processing, the HPA-axis (not just in the stress response), neuronal migration, pruning, and other more 'emergent properties' of the system like direct/complex behavior and therefore development of adaptive/mal-adaptive coping mechanisms and the like.

The paragraphs above, that almost-insultingly superficially skim the pathophysiological basis for this disease, could easily be stated in the context of speaking about any of the protein-opathies (Tau, amyloid or alpha-synuclein), bipolar disorder and many other neurolically-based diseases.

A unifying study of the current level of knowledge of affected systems, pooling the wealth of information already known about calcium metabolism, mitochondrial energetics, the neuro-immune and neuro-endocrine links to this neuropsychiatric problem, in a Manhattan project-like structured environment using state-of-the-science medical bioinformatics, would advance medicine in various fields not just applicable to neuropsychiatric disease.

It is to these applied clinical and theoretical research ends that I wish to apply much of my own personal efforts (and will be facilitating along with other research) in my new position as adjunct faculty at the University of Notre Dame and the Indiana University School of Medicine and as Chief of Psychiatry at Madison Center & Hospitals.

Thoughts?

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