Breakdown of cellular membranes is a characteristic feature of neuronal degeneration in acute (stroke) and chronic (senile dementia) neurological disorders. The present review summarizes recent experimental and clinical work which concentrated on changes of choline-containing phospholipids as indicators of neuronal membrane breakdown. Experimental studies identified glutamate release, calcium influx, and activation of cellular phospholipase A2 (PLA2) as important steps initiating membrane breakdown in cultured neurons or brain slices under hypoxic or ischemic conditions. Proton NMR studies have shown an elevation of choline-containing compounds in the brain of Alzheimer patients while neurochemical studies in post mortem-brain demonstrated increases of the catabolic metabolite, glycerophosphocholine, an indicator of PLA2 activation. In contrast, studies of cerebrospinal fluid, phosphorus NMR studies, and measurements of phospholipases in post mortem Alzheimer brain gave ambiguous results which may be explained by methodical limitations. The finding that, in experimental studies, choline was a rate-limiting factor for phospholipid biosynthesis has stimulated clinical studies aimed at counteracting phospholipid breakdown, e.g. by combinations of choline and cytidine. Future experimental approaches should clarify whether loss of membrane phospholipids is cause or consequence of the neurodegenerative disease process.
"The Cho signal is mainly due to the presence of free glycerophosphocholine and phosphocholine. These compounds are immobile when part of the cellular membrane, but they become mobile and contribute to the Cho signal when the cell membrane has broken down . There are publications reporting an increase of Cho in AD subjects  . "
[Show abstract][Hide abstract] ABSTRACT: Background: The application of non-invasive proton magnetic resonance spectroscopy (1H-MRS) could potentially identify changes in cerebral metabolites in the patients with Alzheimer's disease (AD). However, whether these metabolites can serve as biomarkers for the diagnosis of AD remains unclear. Objective: Using meta-analysis, we aimed to investigate the patterns of cerebral metabolite changes in several cerebral regions that are strongly associated with cognitive decline in AD patients. Methods: Using Hedges' g effect size, a systematic search was performed in PubMed, Cochrane Library, Ovid, Embase, and EBSCO, and 38 studies were integrated into the final meta-analysis. Results: According to the observational studies, N-acetyl aspartate (NAA) in AD patients was significantly reduced in the posterior cingulate (PC) (effect size (ES) = -0.924, p<0.005) and bilateral hippocampus (left hippocampus: ES = -1.329, p<0.005; right hippocampus: ES = -1.287, p<0.005). NAA/Cr (creatine) ratio decreased markedly in the PC (ES = -1.052, p<0.005). Simultaneously, significant elevated myo-inositol (mI)/Cr ratio was found not only in the PC but also in the parietal gray matter. For lack of sufficient data, we failed to elucidate the efficacy of pharmacological interventions with the metabolites changes. Conclusion: The available data indicates that NAA, mI, and the NAA/Cr ratio might be potential biomarkers of brain dysfunction in AD subjects. Choline (Cho)/Cr and mI/NAA changes might also contribute toward the diagnostic process. Thus, large, well-designed studies correlated with cerebral metabolism are needed to better estimate the cerebral extent of alterations in brain metabolite levels in AD patients.
"The Cho/Cr metabolite ratio is thought to represent membrane turnover, as the choline peak is considered to be the breakdown products of phosphatidylcholine – one of the principle components of the cell membrane's phospholipid bilayer (Klein, 2000). Changes in the Cho/Cr ratio in AD dementia have inconsistently been reported to be elevated (Pfefferbaum et al., 1999; Kantarci et al., 2004) or show no change (Moats et al., 1994; Schuff et al., 1997; Rose et al., 1999; Krishnan et al., 2003). "
"As described earlier, brain injury may cause severe neuronal damage and consequent impairment in memory, learning, and motor coordination, and supplementation of omega-3 FAs might be able to reduce the neuronal damage. Neural trauma is usually associated with irregular phospholipid metabolism of neuronal membrane. Omega-3FAs are the major constituents of the membrane phospholipids, which suggests that supplementation of PUFAs could help in reducing the irregular phospholipid metabolism that occurs during neuronal damage. "
[Show abstract][Hide abstract] ABSTRACT: Traumatic brain injury (TBI) is an acquired brain trauma that occurs when any sudden trauma/injury causes damage to the brain. TBI is characterized by tissue damage and imbalance in the cerebral blood ﬂ ow and metabolism. It has been established through laboratory experiments that the dietary supplementation of omega-3 fatty acids (FAs) could reduce the oxidative stress developed in brain due to TBI. The inclusion of omega-3 FA in diet could normalize the levels of brain-derived neurotrophic factor (BDNF), and thus, it could
restore the survival and plasticity of neuronal cells. BDNF improves the synaptic transmission by regulating synapsin 1 and cyclic
adenosine monophosphate (cAMP) response element binding protein. The brain tissue analysis of TBI models supplemented with omega-3 polyunsaturated fatty acids (PUFAs) showed signiﬁ cantly reduced lipid peroxidation, nucleic acid and protein oxidation, thereby promoting neuronal and glial cell survival. Thus, omega-3 FA intake could be considered as a therapeutic option to reduce the secondary neuronal damages initiated by TBI.
Journal of Traditional and Complementary Medicine 04/2014; 4(2):00-00. DOI:10.4103/2225-4110.130374
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