Piracetam, the prototype of the so-called nootropic drugs' is used since many years in different countries to treat cognitive impairment in aging and dementia. Findings that piracetam enhances fluidity of brain mitochondrial membranes led to the hypothesis that piracetam might improve mitochondrial function, e.g., might enhance ATP synthesis. This assumption has recently been supported by a number of observations showing enhanced mitochondrial membrane potential, enhanced ATP production, and reduced sensitivity for apoptosis in a variety of cell and animal models for aging and Alzheimer disease. As a specific consequence, substantial evidence for elevated neuronal plasticity as a specific effect of piracetam has emerged. Taken together, this new findings can explain many of the therapeutic effects of piracetam on cognition in aging and dementia as well as different situations of brain dysfunctions.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944646PMC
http://dx.doi.org/10.3389/fnins.2010.00044DOI Listing

Publication Analysis

Top Keywords

mitochondrial function
8
aging alzheimer
8
alzheimer disease
8
aging dementia
8
piracetam
6
improved mitochondrial
4
function brain
4
aging
4
brain aging
4
disease mechanism
4

Similar Publications

Precise imaging of noncoding RNAs (ncRNAs) in specific organelles allows decoding of their functions at subcellular level but lacks advanced tools. Here we present a DNA-based nanobiotechnology for spatially selective imaging of ncRNA (e.g.

View Article and Find Full Text PDF

Nonantibiotic strategies are urgently needed to treat acute drug-resistant bacterial pneumonia. Recently, nanomaterial-mediated bacterial cuproptosis has arisen widespread interest due to its superiority against antibiotic resistance. However, it may also cause indiscriminate and irreversible damage to healthy cells.

View Article and Find Full Text PDF

The endocannabinoid system (ECS), regulating such processes as energy homeostasis, inflammation, and muscle function, centers around cannabinoid receptors, including CB1. These receptors are mainly located in the central nervous system and skeletal muscles. Hyperactivity of CB1 receptors is linked to metabolic disorders and chronic inflammation, highlighting their potential as therapeutic targets for muscle hypertrophy and metabolic health.

View Article and Find Full Text PDF

Liposomes-Loaded miR-9-5p Alleviated Hypoxia-Ischemia-Induced Mitochondrial Oxidative Stress by Targeting ZBTB20 to Inhibiting Nrf2/Keap1 Interaction in Neonatal Mice.

Antioxid Redox Signal

January 2025

Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.

Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.

View Article and Find Full Text PDF

The mechanisms that drive placental dysfunction in pregnancies complicated by hypoxia and fetal growth restriction remain poorly understood. Changes to mitochondrial respiration contribute to cellular dysfunction in conditions of hypoxia and have been implicated in the pathoaetiology of pregnancy complications, such as pre-eclampsia. We used bespoke isobaric hypoxic chambers and a combination of functional, molecular and imaging techniques to study cellular metabolism and mitochondrial dynamics in sheep undergoing hypoxic pregnancy.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!