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Oxidative-stress has been implicated in Alzheimer’s disease and it is potentially driven by the depletion of primary antioxidant, glutathione, as well as elevation of the pro-oxidant, iron. Present study evaluates glutathione level by magnetic resonance spectroscopy, iron deposition by quantitative susceptibility mapping in left hippocampus as well as the neuropsychological scores of healthy-old participants (N = 25), mild cognitive impairment (N = 16) and Alzheimer’s disease patients (N = 31). Glutathione was found to be significantly depleted in mild cognitive impaired (p < 0.05) and Alzheimer’s disease patients (p < 0.001) as compared to healthy-old participants. A significant higher level of iron was observed in left hippocampus region for Alzheimer’s patients as compared to healthy old (p < 0.05) and mild cognitive impaired (p < 0.05). Multivariate receiver-operating curve analysis for combined glutathione and iron in left hippocampus region provided diagnostic accuracy of 82.1%, with 81.8% sensitivity and 82.4% specificity for diagnosing Alzheimer’s disease patients from healthy-old participants. We conclude that tandem glutathione and iron provides novel avenue to investigate further research in Alzheimer’s disease.

Background: Oxidative stress plays a major role in Alzheimer’s disease (AD) pathogenesis, and thus, antioxidant glutathione (GSH) has been actively investigated in mitigating the oxidative load. Significant hippocampal GSH depletion has been correlated with cognitive impairment in AD. Furthermore, postmortem studies indicated alterations in cellular-energy metabolism and hippocampal pH change toward alkalinity in AD. Objective: Concurrent analysis of hippocampal GSH and pH interplay in vivo on the same individual is quite unclear and hence requires investigation to understand the pathological events in AD. Methods: Total 39 healthy old (HO), 22 mild cognitive impairment (MCI), and 37 AD patients were recruited for hippocampal GSH using 1H-MRS MEGA-PRESS and pH using 2D 31P-MRSI with dual tuned (1H/31P) transmit/receive volume head coil on 3T-Philips scanner. All MRS data processing using KALPANA package and statistical analysis were performed MedCalc, respectively and NINS-STAT package. Results: Significant GSH depletion in the left and right hippocampus (LH and RH) among MCI and AD study groups as compared to HO was observed, whereas pH increased significantly in the LH region between HO and AD. Hippocampal GSH level negatively correlated with pH in both patient groups. The ROC analysis on the combined effect of GSH and pH in both hippocampal regions give accuracy for MCI (LH: 78.27%; RH: 86.96%) and AD (LH: 88%; RH: 78.26%) groups differentiating from HO. Conclusion: Outcomes from this study provide further insights to metabolic alterations in terms of concurrent assessment of hippocampal GSH and pH levels in AD pathogenesis, aiding in early diagnosis of MCI and AD.

: COVID-19 outbreak is one of the most disastrous respiratory diseases (after the 1918 influenza outbreak) spreading in the community. So far, it has killed 7,37,417 number of individuals. High variability in the viral genome and its greater ability to spread in the human community is badly affecting the comorbid individuals. Although infected individuals are mainly possessing respiratory issues, neurological manifestations in these individuals cannot be overlooked. The literature search is based on the recent development in the concerned field. We searched databases like PubMed, Google Scholar, and ScienceDirect using the keywords “COVID-19”, “neurological manifestations”, “CNS”, and “PNS”. The major neurological complications observed in these patients are encephalitis, necrotising haemorrhagic encephalopathy, Guillain Barre Syndrome, smell/taste impairment, epileptic seizures, and abnormal states of consciousness. COVID-19 infection is just more than a cough, fever, and respiratory illness; it can cause indirect neurological complications in infected patients. It is therefore advised to treat and have a careful observation of the COVID-19 patients for neurological manifestations.

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