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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
School of Medical & Allied Sciences, K.R. Mangalam University, Gurugram, Haryana, India.
Background: Parkinson's disease is a hypokinetic disorder characterized by selective loss of dopaminergic in substantia nigra pars compacta (SNPc) region of mid-brain. Dopaminergic degeneration of neurons is considered to be due to oxidative stress, neuroinflammation, neurons mitochondrial dysfunction and glutamate excitotoxicity etc. Inosine a purine nucleoside has been reported to produce anti-oxidant, anti-inflammatory and neuromodulatory actions in previous studies.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Background: Mitochondria are organelles where energy production takes place via oxidative phosphorylation, thus mitochondrial function influences the organs with large energy consumption, such as the brain. Mitochondria contain their own circular genome (mtDNA), which encodes essential proteins/RNAs involved in oxidative phosphorylation. The maternal inheritance of mtDNA, combined with a higher risk of Alzheimer's disease (AD) observed in females, suggest mtDNA may have a role in AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Oxford, Oxford, United Kingdom.
Background: Alzheimer's (AD) and Parkinson's disease (PD) feature progressive neurodegeneration in a remarkably regionally selective manner. Post mortem studies have posited a role for cell autonomous mechanisms driving this, so we aimed to examine a live human induced pluripotent stem cell (iPSC) model to see whether it can replicate the phenomenon of selective neuronal vulnerability, so to better determine disease mechanisms and therapeutic targets.
Method: iPSC-derived neurons offer a rare opportunity to examine cell autonomous vulnerability in live human cells.
From Ca dysregulation to heart failure: β-adrenoceptor activation by RKIP postpones molecular damages and subsequent cardiac dysfunction in mice carrying mutant PLN by correction of aberrant Ca-handling.
Pharmacol Res
December 2024
Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Str. 9, 97078 Würzburg, Germany; Leibniz-Institut für Analytische Wissenschaften - ISAS - e.V., Bunsen-Kirchhoff-Str. 11, 44139 Dortmund, Germany; Comprehensive Heart Failure Center, University Hospital of Würzburg, Am Schwarzenberg 15, 97078 Würzburg, Germany. Electronic address:
Article Synopsis
- Impaired calcium (Ca) handling in heart cells is a key feature of heart failure (HF), leading to issues like weakened heart contractions and irregular heartbeats.
- The study used transgenic mice with a mutation affecting a calcium regulator (phospholamban) to understand how defects in calcium cycling contribute to HF, noting that these mice experience severe and fast-progressing heart failure.
- Early treatment aimed at correcting calcium cycling using Raf kinase inhibitor protein (RKIP) was found to delay heart cell damage and improve overall health of the mice, indicating that addressing Ca dynamics early on could be crucial for preventing further complications in heart failure.
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