From basic neuronal survival to specialized function, oscillation and higher brain activity
Suggested URL: /neurological-function-cellular-energy/ | Parent: Human Health and the ACE Pathway
The Brain Has Exceptional Energy Requirements
Neurons must maintain membrane potentials, generate electrical activity, restore ionic gradients, synthesize and recycle signaling components, and coordinate activity across large networks.
A neuron can therefore remain alive while failing to perform its specialized function adequately. This distinction between cellular survival and specialized function is central to the proposed concept of Insufficiency of Cellular Energy (ICE).
Two Proposed Roles for Brain Electrical Activity
Electrical oscillations have established roles in neuronal communication and network coordination.
The KELEA hypothesis proposes a second, distinct possibility: repetitive changes in electrical-charge separation may also allow neurons and neuronal networks to receive or concentrate KELEA.
In this model, neural oscillation could have both an INFORMATIONAL function and a proposed ENERGETIC function.
An Evolutionary Hypothesis
An advanced hypothesis is that oscillatory electrical activity may have provided an energetic advantage even in early excitable cells and simple nervous systems, before increasingly complex neural networking evolved.
If changing electrical-charge relationships can attract KELEA, rhythmic depolarization could theoretically have served as a biological Enerceutial. More elaborate nervous systems could then have developed both the energetic and networking properties of electrical activity.
This is a hypothesis for investigation, not an established account of nervous-system evolution.
Frequency May Matter
The proposed KELEA interaction need not be viewed simply as “more energy is better.”
If KELEA couples to changing charge relationships, the frequency, amplitude, pattern and coherence of those changes may influence coupling. Gamma-range brain activity is one possible area for investigation, but no particular human brain frequency has been established as a KELEA-receiving frequency.
This leads to a testable question: do different controlled patterns of electrical oscillation differ in their ability to produce measurable Enerceutial effects?
Neurodevelopmental and Neurodegenerative Branches
The neurological roadmap divides naturally into two major clinical branches.
NEURODEVELOPMENTAL
Autism and related observations
Epilepsy within the earlier clinical work
Development of specialized brain function
NEURODEGENERATIVE
Alzheimer’s disease
Parkinson’s disease
ALS and other disorders
Aging and maintenance of neuronal function
The evidence and proposed mechanisms differ among these conditions and should be considered on separate pages.
Alzheimer’s Disease as a Model
A 2017 paper proposed that some neurons in Alzheimer’s disease may become functionally quiescent from insufficient cellular energy before they are irreversibly lost.
The important distinction is between a DEAD neuron and a VIABLE BUT FUNCTIONALLY INADEQUATE neuron. If such a reversible stage exists, cellular energy becomes a potentially testable variable.
The ACE/KELEA explanation remains a hypothesis; the observation that specialized neuronal function requires substantial energy is the conventional biological starting point.
Higher Brain Functions
The ACE hypothesis also raises a more exploratory possibility: additional available energy may contribute to higher levels of organized brain function rather than merely preventing energetic failure.
Attention, cognition, creativity and emotional states—including the possibility of joy—can eventually be considered as research questions involving organized neural activity. They should not be presented as established consequences of KELEA.
Selected Published Sources
Martin WJ. Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway. Advances in Alzheimer’s Disease. 2017;6:1-12. DOI 10.4236/aad.2017.61001.