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Attwell, D. and Laughlin, S.B. (2001) An Energy Budget for Signaling in the Grey Matter of the Brain. Journal of Cerebral Blood Flow & Metabolism, 21, 1133-1145.
https://doi.org/10.1097/00004647-200110000-00001

has been cited by the following article:

  • TITLE: Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

    AUTHORS: W. John Martin

    KEYWORDS: Alzheimer’s Disease, Alternative Cellular Energy, ACE, Insufficiency of Cellular Energy, ICE, Kinetic Energy Limiting Electrostatic Attraction, KELEA, Homeopathy, Enercel, Enerceutical, Calorie, Metabolism, Electrical Charge, Membrane Potential, Neurodegeneration, Psychiatry

    JOURNAL NAME: Advances in Alzheimer's Disease, Vol.6 No.1, March 2, 2017

    ABSTRACT: The term neurodegeneration emphasizes the destruction of neuronal cells as the primary explanation of many major neurological illnesses, including Alzheimer’s disease. Specialized functioning of cells requires more cellular energy than is needed for basic cell survival. Cells can acquire energy both from the metabolism of food and from the alternative cellular energy (ACE) pathway. The ACE pathway is an added dynamic (kinetic) quality of the body’s fluids occurring from the absorption of an external force termed KELEA (Kinetic Energy Limiting Electrostatic Attraction). KELEA is attracted to separated electrical charges and is seemingly partially released as the charges become more closely linked. As suggested elsewhere, the fluctuating electrical activity in the brain may attract KELEA from the environment and, thereby, contribute to the body’s ACE pathway. Certain illnesses affecting the brain may impede this proposed antenna function of the brain, leading to a systemic insufficiency of cellular energy (ICE). Furthermore, individual neurons may derive some of the energy for their own activities from the repetitive depolarization of the cell. This may explain why hyper-excitability of neurons can occur in response to cell damage. This adaptive mechanism is unlikely to be sustainable, however, especially if there is a continuing need to synthesize neurotransmitters and membrane ion channels. The energy deficient neurons would then become quiescent and, although remaining viable, would not perform their intended specialized functions. Actual cell death would not necessarily occur till much later in the disease process. The distinction between quiescent and degenerated cells is important since the ACE pathway can be enhanced by several means, including the regular consumption of KELEA activated water. This, in turn, may improve the proposed antenna function of individual neurons, leading to a sustained restoration of specialized function via the ACE pathway. This paper explores this novel concept and provides a rationale for clinical testing of KELEA activated water in patients with neurological and psychiatric illnesses, including Alzheimer’s disease.