Anna is Jerry’s mother. She had neuromuscular weakness as a child and did not walk till the age of 4. Her siblings had neuromuscular problems as well, some more severe, some less. Two of her siblings died from heart failure in infancy and early childhood.
Anna lived to be 90 but she developed altered mental status at the age of 85 when her kidney function began to fail by a lot. She was put on dialysis and received erythropoietin To Jerry’s surprise, the function of her mind improved a lot. Suddenly she was able to recall and discuss facts of news article she read, something she had not been able to do for decades. She was also quick to learn new technologies, again, something she’d had difficulty with for some time. It was as if her brain cells had been dormant for years, and with this treatment for her blood [erythropoietin] and with proper artificial kidney function, these dormant cells began to work. Her mind functioned as it must have functioned at her prime, in her twenties. It was amazing to witness.
Dialysis is no fun and she did suffer but the main point is that, short of a stroke, it seems that scientists have a lot to learn about higher brain function and how to bring back brain function that has been “muted” rather than destroyed.
Muted function of the mind and of spontaneous thought, speech and voluntary action may look like depression, insanity even partial or complete dementia and we need to study the conditions in which we might be able to restore these functions. This is what we observed in Anna’s case, in Jerry’s case and in Paula’s case and in the thousands of patients followed by Kraepelin.
We never measured Anna’s breathing rate at rest. We did not think of it.It is possible that her breathing at rest was abnormal and contributed to the eventual failure of the kidneys. Who knows?
We have looked at other patients with partial dementia and disturbed breathing at rest. One had severe heart failure and much undiagnosed too fast breathing at rest. He never got medical support to help him breath. He suffered a lot. He didn’t know he had altered mental status and no one else [except us] noticed. Another patient we know had too slow breathing [almost 8 breaths per minute at rest] for a long time before she developed Parkinson’s. Ironically, the medication to control the tremors also changed her breathing rate to upper normal at rest [20 breaths per minute]. We could give lots of other examples of abnormal breathing rates at rest and subsequent illness but we won’t.
We are just beginning to learn how animals deal with anoxia and the role of the mitochondria in managing fluctuations of oxygen tension in the environment or in illness.
A revolution in our understanding of brain development, adult brain function, senescence, and disease has emerged from the recognition of structural and functional plasticity within the mammalian brain (1). For example, the role of brain-derived neurotrophic factor (BDNF) and other hormonal factors that mediate neurogenesis, as well as synaptic and dendritic plasticity in psychiatric disorders (2), has revealed unforeseen neuronal regulatory mechanisms. These build on a growing dynamic conception of brain architecture that complements the understanding of synaptic transmission. This, we are also discovering, is a plastic event altered by both structural and functional remodeling of the synapse. However, little is known about the role of mitochondria in regulating synaptic transmission, and less yet about their implications for cognitive function and memory decline in the aging brain (3). The study by Hara et al. (4) in PNAS synergizes with recent discoveries, revealing a key role of mitochondria regulating synaptic transmission, brain function, and cognition in aging.
Mitochondria populate the cytoplasm of mammalian cells, including neurons, which rely on mitochondrial energy production for survival. These organelles contain their own genome—the mitochondrial DNA (mtDNA)—which encodes essential subunits of the respiratory chain where electrons are combined with oxygen to enable the flow of energy through mitochondria. Energized mitochondria can then synthesize ATP that fuels energy-dependent intracellular reactions (such as endocytosis, ion transport, and neurotransmitter biosynthesis) and sustain other critical mitochondrial functions [Ca2+ handling, reactive oxygen species (ROS) production, and others], contributing to intracellular signaling (5). Equally important is the relatively recent discovery that mitochondria dynamically undergo shape changes through regulated processes of fusion and fission (making longer or shorter organelles, respectively) and actively traffic between cell compartments such as the soma, axon, and presynaptic boutons (6). Mitochondria impact brain function and cognition Martin Picard and Bruce S. McEwen PNAS January 7, 2014 111 (1) 7-8
It bears repeating, ……we are just beginning to learn how animals deal with anoxia and the role of the mitochondria in managing fluctuations of oxygen tension in the environment or in illness…….regular respiratory rate at rest and during sleep , tidal volume, dead space and alveolar ventilation ….all of this is important and we seem not to understand the half of it. But I propose that it is all very important to the flow of energy through the mitochondria and to their switch to reversible energy saving states. Energy saving states that “mute” function of the mind, until conditions improve enough to flip back to normal.
Of Sound Mind 