As individuals age, they undergo both biological and physiological changes that are apparent and expected. Another often overlooked aspect of senescence are the changes in cognition and behaviour. The Show more
As individuals age, they undergo both biological and physiological changes that are apparent and expected. Another often overlooked aspect of senescence are the changes in cognition and behaviour. These are often misunderstood or complicated with common neurodegenerative disorders found in the elderly. This chapter acts as an introduction into these cognitive-behavioural changes. There are a variety of methodologies currently employed in the investigation of these changes, such as functional magnetic resonance imaging, electroencephalography, and animal studies. Novel methodologies are being deployed for the analysis of gut-flora interactions with the CNS and how they may impact behavioural changes as our microbiota changes in late-life. Multiple modulatory factors are at play as well, further complicating the multifaceted nature of ageing cognition differences. Sex and genetics are major factors that are associated with age-related behavioural changes. Gross structural and molecular changes in the CNS are also associated with pronounced changes in cognition. Low-grade chronic inflammation, epigenetics and infections also seem to be significant. Neurodegenerative diseases, whilst pathological, work in tandem with natural ageing and present age-related changes in behaviour. The most common changes are summarised and the expression of the previously discussed modulatory factors are presented. Show less
Atherosclerosis is a chronic condition characterized by impaired lipid homeostasis and chronic inflammatory pathology in large and mid-sized arteries. Myocardial infarction is caused by coronary arter Show more
Atherosclerosis is a chronic condition characterized by impaired lipid homeostasis and chronic inflammatory pathology in large and mid-sized arteries. Myocardial infarction is caused by coronary artery thrombosis in a ruptured or unstable atherosclerotic plaque. Despite the emphasis on known triggering factors, such as hypertension and dyslipidemia, adverse events following MI, such as recurrence and mortality, are still high. Therefore, it is imperative to assess potential determinants of plaque instability. We evaluated markers of inflammation, extracellular matrix (ECM) remodeling, thrombosis, and lipids in first-time and recurrent MI (RMI). Two hundred patients diagnosed with MI within the first 24 h of the event were included in the study and categorized as first-time or recurrent MI. Serum levels of NF-κB, hs-CRP, TNF-α, IFN γ, IL-6, VCAM-1,MMP-9, stromelysin, TIMP-1, MCP-1, PAPP-A, vWF, D-dimer, PLA2, PON-1, Apo-B, Apo-A1, ox-LDL, and anti-oxidized LDL antibodies were analyzed by ELISA. We performed a multivariate logistic regression analysis for risk stratification. The mean age of first-time MI patients was 52.4 ± 25 years and that of recurrent MI patients was 55.9 ± 24.6 years. RMI patients showed significant ( Non-lipid factors provide substantial insights into plaque instability. Multiple markers of inflammation, thrombosis, extracellular matrix remodeling, and paroxonase-1 are reliable indicators of recurrent myocardial infarction. Show less