Aims: To evaluate prospective memory (PM) functioning in early breast cancer (BC) survivors and its association with fatigue and depression.
Methods: The Memory for Intention Screening Test, the Center for Epidemiologic Studies Depression Scale and the Functional Assessment of Cancer Therapy-Fatigue subscale were administered to 80 patients and 80 aged-matched healthy controls.
Results: Patients performed more poorly than controls on the memory test (p < 0.001) and had a higher rate of impairment (odds ratio = 5.5, p < 0.01). Fatigue mediated the relationship between Group membership and PM performance.
Conclusions: BC survivors exhibited a clear pattern of PM deficit and fatigue was a major contributor to this deficit. This suggests that a common mechanism may be involved in fatigue symptoms and memory disturbances experienced by patients. Further research is needed to evaluate the role of adjuvant therapy in PM deficits and to explore whether interventions targeted at improving fatigue may also improve memory functioning in BC survivors.
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http://dx.doi.org/10.1016/j.breast.2013.04.002 | DOI Listing |
Stem Cells
January 2025
Bioengineering Graduate Program, University of Notre Dame, Notre Dame, 46556 IN, USA.
Myocardial infarction can lead to the loss of billions of cardiomyocytes, and while cell-based therapies are an option, immature nature of in vitro-generated human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCMs) is a roadblock to their development. Existing iPSC differentiation protocols don't go beyond producing fetal iCMs. Recently, adult extracellular matrix (ECM) was shown to retain tissue memory and have some success driving tissue-specific differentiation in unspecified cells in various organ systems.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFAge Ageing
January 2025
Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Background: A mobile cognition scale for community screening in cognitive impairment with rigorous validation is in paucity. We aimed to develop a digital scale that overcame low education for community screening for mild cognitive impairment (MCI) due to Alzheimer's disease (AD) and AD.
Methods: A mobile cognitive self-assessment scale (CogSAS) was designed through the Delphi process, which is feasible for the older population with low education.
Front Biosci (Landmark Ed)
January 2025
Department of Zoology, College of Science, King Saud University, 11451 Riyadh, Saudi Arabia.
Background: We investigated chitosan's protective effects against tertiary butylhydroquinone (TBHQ)-induced toxicity in adult male rats, focusing on cognitive functions and oxidative stress in the brain, liver, and kidneys.
Methods: Rats were divided into four groups (n = 8/group): (1) Control, (2) Chitosan only, (3) TBHQ only, and (4) Chitosan + TBHQ.
Results: TBHQ exposure led to significant cognitive impairments and increased oxidative stress, marked by elevated malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and glutathione (GSH) levels.
Front Biosci (Landmark Ed)
January 2025
HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Danube Neuroscience Research Laboratory, H-6725 Szeged, Hungary.
Backgrounds: Memory and emotion are especially vulnerable to psychiatric disorders such as post-traumatic stress disorder (PTSD), which is linked to disruptions in serotonin (5-HT) metabolism. Over 90% of the 5-HT precursor tryptophan (Trp) is metabolized via the Trp-kynurenine (KYN) metabolic pathway, which generates a variety of bioactive molecules. Dysregulation of KYN metabolism, particularly low levels of kynurenic acid (KYNA), appears to be linked to neuropsychiatric disorders.
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