Aging and beta-amyloid peptides decrease cholinergic receptor-mediated calcium increase in brain cortex synaptoneurosomes.

M Samochocki

doi:10.55782/ane-1998-1253

Home/Archive/PubMed

PubMed · 9583182

Aging and beta-amyloid peptides decrease cholinergic receptor-mediated calcium increase in brain cortex synaptoneurosomes.

M Samochocki

View original source ↗Export metadata ↓

Abstract

In this study, the muscarinic cholinergic receptor (MAChR)-evoked inositol 1,4,5-trisphosphate (IP3)-mediated increase of cytosolic calcium concentration ([Ca]i) in synaptoneurosomes from brain cortex of adult and aged rats was investigated. In addition, the effect of two beta-amyloid (A beta) peptides, 1-28 and 25-35, on the resting and MAChR-induced increase of [Ca]i in brain cortex synaptoneurosomes of adult rats was evaluated. Release of IP3 was measured after prelabeling of synaptoneurosomal phosphoinositides with myo-[2-3H]inositol. Changes in [Ca]i were monitored by using fura-2 indicator. The effect of A beta peptides was evaluated following their preincubation with synaptoneurosomal protein for 1, 5, 30 and 60 min. It was observed that in brain cortex synaptoneurosomes from aged rats, Ca(2+)-dependent and MAChR-mediated IP3 production was not changed in comparison with that estimated in adult brain, over 60 min of incubation. Activation of MAChR in synaptoneurosomes from brain cortex of adult rats for 10 min increased [Ca]i by about 60% over its resting level (240 nM). This increase was completely blocked by muscarinic antagonists, atropine and pirenzepine, as well as by the antagonist of IP3 receptor, 8-(diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8). In aged brain, there was no detectable change in resting [Ca]i (165 nM) due to MAChR stimulation. The 25-35 A beta peptide caused a time-dependent significant increase of resting [Ca]i in synaptoneurosomes from brain cortex of adult rats, which was almost five-fold after 60 min. In the same conditions, the action of 1-28 A beta peptide was statistically insignificant up to 30 min, then a rapid increase of resting [Ca]i by two-fold was observed up to 60 min. Both A beta peptides decreased markedly the MAChR-dependent elevation of [Ca]i in respect to control (resting [Ca]i) in synaptoneurosomes from brain cortex of adult rats. These results indicate that beta-amyloid 1-28 and 25-35 peptides may be involved in alteration of muscarinic receptor-mediated signal transduction during brain aging.

Explore related subjects

Aging Amyloid beta-Peptides Animals Calcium Cerebral Cortex In Vitro Techniques Neuropeptides Rats Receptors, Cholinergic Synaptosomes Journal Article Research Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

M Samochocki. 1998. Aging and beta-amyloid peptides decrease cholinergic receptor-mediated calcium increase in brain cortex synaptoneurosomes.. https://doi.org/10.55782/ane-1998-1253

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

An open benchmark and language models for AI in aging biology.

Over the past two decades, human aging has been characterized across DNA methylation, transcriptomic, proteomic, and clinical modalities, yet no benchmark evaluates whether AI systems can interpret these heterogeneous data types in the context of aging biology. We introduce LongevityBench, an open suite of 17 tasks spanning five biodata domains, and use it to assess 18 frontier AI systems from six developer teams. Despite recent advances in AI, no single model dominates all tasks, with omics-based age prediction being the hardest task regardless of scale. To test whether these gaps can be closed without frontier-scale resources, we fine-tuned a family of five multitask Longevity-LLMs on domain-specific aging data. The compact (0.6B-9B parameters) Longevity-LLMs matched or exceeded far larger frontier systems on LongevityBench, showing that general-purpose language models can be adapted to structured-omics tasks. We publicly release the benchmark, models, and Longevity Claw, an agentic research interface for aging researchers.

Aging↗

PubMed2026

Association between sirtuin 1 and markers of oxidative stress in master athletes.

BACKGROUND: Lifelong training in master athletes confers protective effects, promoting higher sirtuin levels and enhanced antioxidant capacity. Although Sirtuin 1 (SIRT1) is well studied, no previous study has examined the relationship between circulating SIRT1 levels and antioxidant defense variables in master athletes. PURPOSE: To compare and analyze the relationships between circulating levels of SIRT1 and variables related to antioxidant defense in master athletes (MA) and untrained middle-aged individuals (UMA). METHODS: Male MA (n = 42; 51.62 ± 7.33 years; ≥10 years of training and competition in running) and UMA (n = 15; 47.73 ± 8.52 years) were evaluated. Venous blood samples were collected for biochemical analyses of SIRT1, antioxidant enzymes, TBARS and F2-isoprostanes, 8-OHdG, and redox balance indexes. RESULTS: MA showed higher levels of SIRT1 (18.22 ± 4.53 vs. 6.08 ± 2.11 ng/mL; p < 0.0001), as well as of SOD, CAT, and GSH (p < 0.001), indicating a more favorable antioxidant profile. After adjustment for body fat percentage, differences in SOD, CAT, GSH and TBARS, remained significant. SIRT1 was positively correlated with SOD (r = 0.279; p = 0.031), CAT (r = 0.485; p < 0.001), GSH (r = 0.476; p < 0.001) and CAT/8-OHdG (r = 0.430; p = 0.032), and negatively correlated with TBARS (r = - 0.518; p < 0.001). CONCLUSION: Master athletes exhibited higher circulating SIRT1 concentrations and a more favorable systemic redox profile than untrained individuals, with SIRT1 being associated with markers of antioxidant defense, lipid peroxidation, and redox balance.

Aging↗

PubMed2026

Decoding SUMOylation as a metabolic stress sensor in aging and age-related disorders: Mechanisms, tissue specificity and therapeutic potential.

SUMOylation is a reversible post-translational modification increasingly recognized for its role in coordinating cellular responses to metabolic stress during aging. Emerging evidence indicates that it functions beyond a conventional modification, representing an adaptive stress‑responsive regulatory network that integrates metabolic, oxidative, inflammatory, and proteotoxic signals. Rather than acting on isolated pathways, this network finely tunes mitochondrial function, proteostasis, genome maintenance, immune balance, and epigenetic regulation. Accumulating evidence indicates that SUMO-dependent regulation exhibits remarkable tissue specificity, supporting mitochondrial adaptation and contractile integrity in skeletal muscle, shaping lipid and glucose metabolism in the liver, modulating proteotoxic stress and neuronal resilience in the brain, and contributing to immune cell differentiation and chronic low-grade inflammation during aging. In this review, we summarize current mechanistic insights into SUMO signaling across aging-relevant tissues, with particular emphasis on its functional interplay with other post-translational modifications, including ubiquitination and acetylation. We discuss how SUMOylation operates as a shared regulatory layer while enabling context-dependent outcomes that underlie diverse aging phenotypes and age-related disorders. Finally, we evaluate emerging translational approaches-ranging from pharmacological modulation of SUMO enzymes to lifestyle interventions such as caloric restriction and exercise-that highlight both the opportunities and challenges of targeting SUMO-regulated stress responses in aging. Together, this synthesis provides a framework for understanding how SUMOylation links metabolic stress to tissue-specific aging trajectories and therapeutic potential.

Aging↗