The cerebral atrophy resulting from the death of neurons is the dominant change in BA patients (AI Oifa, 1987). The cholinergic neurons of the associative parietal, temporal and frontal areas of the cortex, the basal nucleus of Meynert, the hippocampus and the tonsils, and the noradrenergic neurons of the blue spot are most affected (E. Masliah, L. Hansn, 1994). Amyloid angiopathy is expressed in small and medium vessels of the cortex (DD Orlovskaya, AI Oifa, 1984).
Most authors who have studied energy metabolism in patients with asthma indicate a decrease in glucose metabolism intensity in the parietal, temporal, and frontal
associative cortical areas with its relative preservation in the primary sensorimotor and visual cortex, as well as in the cerebellum, basal ganglia and thalamus. These changes are expressed even in the early stages of BA (F. Fazekas et al., 1989). In patients with asthma, the relative metabolism of glucose in the associative regions with respect to the projection is much less than normal. In healthy people, this indicator depends on age. Metabolic differences are less noticeable between patients with asthma and old people than between patients with asthma and young subjects. Local cerebral blood flow in associative areas in patients with asthma is reduced, but there is no significant correlation between blood flow rate and asthma severity or age. Due to a decrease in aerobic oxidation and a relative increase in glycolysis in BA, the production of lactate is increased (F. Fazekas et al, 1989; W.Heiss, 1991; N. Azari et al 1994).
Patients with asthma showed disturbances in the work of mitochondria. Cytochrome oxidase activity – the respiratory chain enzyme is reduced, which leads to the “escape” of electrons from the respiratory chain and increased production of oxygen free radicals (S. Chosh et al., 1997). The latter, as inducers of apoptosis, increase atrophy (CW Cotman, CJ Pike, 1997).
According to MRI, with BA reduced the formation of ATP. Energy becomes insufficient to maintain the membrane potentials of the neurons and partial depolarization of the membrane occurs. As a result, even the usual concentrations of the excitatory glutamate mediator cause excessive activation of NMDA receptors, which leads to the accumulation of Ca in the neuron, activation of Ca-dependent endonucleases, lipases and proteases and degradation of cellular structures (M. Beal, 1992; J. Pettegrew et al., 1997).).
With a decrease in energy metabolism
It is assumed that a decrease in energy metabolism plays a key role in the disruption of acetylcholine synthesis, since the precursor of this neurotransmitter, acetyl CoA, is formed in the brain from glucose mainly by the glycolytic route. Disruption of the normal processing of amyloid precursor protein, which is a reparative protein of cell membranes, is also associated with a decrease in energy metabolism. Normally, this protein is integrated into cell membranes and is cut by proteases in the beta region. This process depends on the energy of ATP. With a critical decrease in ATP synthesis in patients with BA, the amyloid precursor protein cannot be integrated into cell membranes and, accordingly, its cleavage in the beta region is impaired. As a result, abnormal processing of the protein occurs, and beta-amyloid is synthesized from its beta fragments,which progressively accumulates in the senile plaques and vascular wall (W. Meiruge et al., 1994).
Although the results of experimental studies indicate the important pathogenetic significance of changes in energy metabolism and brain CNS for the development of asthma, before the advent of computerized visualization methods for cerebral biochemical processes and the analysis of SCP, the study of changes in acid-base balance in the brain in patients with asthma was difficult. In the following sections, changes in the SCP of the brain in patients with Alzheimer’s-type dementia are considered, as well as the relationship of these changes with biochemical and electrophysiological indicators.