Energy Metabolism The Critical Role of Mitochondrial Function Decay

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The human brain, representing less than 2% of the body weight, receives about 16 to 17% of the cardiac output and accounts for about 20% of the total oxygen consumption in resting conditions. From these data it can easily be inferred that routine brain functions are critically dependent on the synthesis of high energy intermediates by neurons and glia, although these two types of nerve cells have different energy requirements and, of course, there are marked differences between their energy demands.

Cerebral energy metabolism in aging has been investigated in animal models and human beings by measuring different parameters, such as cerebral blood flow (CBF) and cerebral metabolic rate for glucose (CMRGlc) or oxygen (CMRO2). Noninvasive techniques have been developed during the past decades beginning in the early 1960s to measure these important parameters. Positron emission tomography (PET) is one of these currently used methods and is based on principles of computerized tomography and radioisotope imaging. Specifically in emission tomography, the image is generated by differences in the distribution in the tissue of injected or inhaled isotopes that are constituents of important biological molecules. The radiation emitted by the isotopes can be detected, analyzed, and used by a computer to visualize the zones where a specific biological molecule is metabolized. In PET, the isotopes of elements that decay after minutes or hours are normally used and emit positrons (positive charged particles similar in mass to electrons). With the exception of severe injury, such as stroke and head trauma, CBF is coupled to cerebral metabolism since neural mechanisms that need energy to be accomplished are also able to modulate the brain's blood perfusion. PET has been used to estimate local rates of CBF and the results obtained documented that in human aging a decrease in this parameter occurs in the limbic system and association areas. This is probably due to the changes that occur with aging in cognitive functions. Other areas of the old human brain appear to be differently affected by a decrease in CBF, but the most commonly observed age-related impairment has been found in the frontal lobes bilaterally. Moreover it has been found that in aging there is a decrease of CBF in gray, but not in white, matter (Leenders et al., 1990). The quantitative estimations of CBF may easily be affected by physiological, psychological, and environmental factors. However, the regional values estimated in each individual are normalized to the whole brain blood flow with the aim of eliminating variations in the measurements of absolute flow. Multiple factors may be responsible for the age-related changes in CBF, and these include a decline in the mechanisms that regulate CBF, alterations of the cerebral blood vessels due to age (e.g., mild amyloid angiopathy), and a decrease of neuron function leading to brain atrophy. The 18F-deoxyglucose is the most commonly used radiopharmaceutical for PET imaging to investigate CMRGlc or CMRO2. In aging, CMRGlc decreases in temporal, parietal, and frontal regions of the brain. CMRO2 also is reported to decrease with advancing age, particularly in the gray matter in subjects over 51 years of age (Takada et al., 1992). The reliability of the results on cerebral metabolism from PET analysis is challenged by measurements of brain atrophy since PET data are the outcome of an average of signals from the brain tissue and CSF spaces (i.e., the spaces occupied by the cerebrospinal fluid), and a marked atrophy may result in a lower PET value. A reasonable suggestion for a correct interpretation of PET data is that changes in brain volume must be considered. Atrophy correction of cerebral metabolism has been carried out in AD studies, and it has been documented that the AD hypometabolism is related to the loss of tissue, whereas the still existing tissue does not show metabolic differences vs. controls. Age-related brain damage and the appearance of potential neuro-pathological signs may depend on causative events leading to an impaired metabolism affecting different groups of neurons in which reduction of energy may result from the decay of the cell's metabolic machinery, that is, from subtle, though significant, mitochondrial dysfunctions.

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