Alzheimer's disease and vascular dementia are the two most common types of dementia with the former being the most predominant. It is evident that oxidative stress, an environment where pro-oxidant species overwhelm antioxidant species, is involved in the pathogenesis of both forms of dementia. An increased level of reactive oxygen species in the vasculature, reduced nitric oxide bioavailability, and endothelial dysfunction leading to vascular disease is associated with vascular dementia. In Alzheimer's disease, an increased amount of amyloid-beta peptide induces elevated reactive oxygen species production thereby causing neuronal cell death and damage. The recent observation that increased atherosclerotic plaque formation is present in the main artery to the brain in Alzheimer's disease, coupled with the association of vascular risk factors with this disease, suggests a link between these two dementias. This review will argue that Alzheimer's disease and vascular dementia are two extremes of one disease, thus assuming a hypothesis where the clinical conditions referred to as dementia are part of a continuum. We propose that the majority of cases share a vascular pathology and that oxidative stress is central to this common pathology.

The purpose of the present study was to compare acute changes in oxidative stress and inflammation in response to steady state and low volume, high intensity interval exercise (LV-HIIE). Untrained healthy males (n = 10, mean ± s: age 22 ± 3 years; VO2MAX 42.7 ± 5.0 ml · kg(-1) · min(-1)) undertook three exercise bouts: a bout of LV-HIIE (10 × 1 min 90% VO2MAX intervals) and two energy-matched steady-state cycling bouts at a moderate (60% VO2MAX; 27 min, MOD) and high (80% VO2MAX; 20 min, HIGH) intensity on separate days. Markers of oxidative stress, inflammation and physiological stress were assessed before, at the end of exercise and 30 min post-exercise (post+30). At the end of all exercise bouts, significant changes in lipid hydroperoxides (LOOH) and protein carbonyls (PCs) (LOOH (nM): MOD +0.36; HIGH +3.09; LV-HIIE +5.51 and PC (nmol · mg(-1) protein): MOD -0.24; HIGH -0.11; LV-HIIE -0.37) were observed. Total antioxidant capacity (TAC) increased post+30, relative to the end of all exercise bouts (TAC (µM): MOD +189; HIGH +135; LV-HIIE +102). Interleukin (IL)-6 and IL-10 increased post+30 in HIGH and LV-HIIE only (P < 0.05). HIGH caused the greatest lymphocytosis, adrenaline and cardiovascular response (P < 0.05). At a reduced energy cost and physiological stress, LV-HIIE elicited similar cytokine and oxidative stress responses to HIGH.

A large body of evidence supports a role of oxidative stress in Alzheimer disease (AD) and in cerebrovascular disease. A vascular component might be critical in the pathophysiology of AD, but there is a substantial lack of data regarding the simultaneous behavior of peripheral antioxidants and biomarkers of oxidative stress in AD and vascular dementia (VaD). Sixty-three AD patients, 23 VaD patients and 55 controls were included in the study. We measured plasma levels of water-soluble (vitamin C and uric acid) and lipophilic (vitamin E, vitamin A, carotenoids including lutein, zeaxanthin, β-cryptoxanthin, lycopene, α- and β-carotene) antioxidant micronutrients as well as levels of biomarkers of lipid peroxidation [malondialdehyde (MDA)] and of protein oxidation [immunoglobulin G (IgG) levels of protein carbonyls and dityrosine] in patients and controls. With the exception of β-carotene, all antioxidants were lower in demented patients as compared to controls. Furthermore, AD patients showed a significantly higher IgG dityrosine content as compared to controls. AD and VaD patients showed similar plasma levels of plasma antioxidants and MDA as well as a similar IgG content of protein carbonyls and dityrosine. We conclude that, independent of its nature – vascular or degenerative – dementia is associated with the depletion of a large spectrum of antioxidant micronutrients and with increased protein oxidative modification. This might be relevant to the pathophysiology of dementing disorders, particularly in light of the recently suggested importance of the vascular component in AD development.

Exercise induces mobilisation of CD8+ T lymphocytes (CD8TL) into the peripheral blood. This response is largely confined to effector-memory CD8TLs: antigen experienced cells which have a strong tissue-homing and effector potential. This study investigated whether effector-memory cells also account for the CD8TL egress from peripheral blood following exercise. As latent Cytomegalovirus (CMV) infection is associated with a robust expansion in the number and proportion of effector-memory CD8TLs, we also investigated if CMV serostatus was a determinant of the CD8TL responses to exercise. Fourteen males (Mean age 35, SD ± 14 yrs), half of whom were CMV seropositive (CMV+), ran on a treadmill for 60 min at 80% V_ O2 max. Blood was collected at baseline, during the final minute of exercise, and 15 min and 60 min thereafter. CD8TL memory subsets were characterised by flow cytometry, using the cell-surface markers CD45RA, CD27, and CD28. The results confirmed that CD8TLswith an effector-memory phenotype (CD27CD28CD45RA+/) exhibited the largest increase during exercise (+200% to +250%), and also showed the largest egress from blood 60 min post-exercise (down to 40% of baseline values). Strikingly, the mobilisation and subsequent egress of total CD8TLs was nearly twice as large in CMV+ individuals. This effect appeared specific to CD8TLs, and was not seen for CD4+ T lymphocytes or total lymphocytes. This effect of CMV serostatus was largely driven by the higher numbers of exercise-responsive effector-memory CD8TLs in the CMV+ participants. This is the first study to demonstrate that infection history is a determinant of immune system responses to exercise

Oxidative stress and inflammation are increased with advancing age. Evidence suggests that oxidative stress and inflammation both lead to impaired vascular function. There is also evidence to suggest that inflammation may cause an increase in radical production leading to enhanced oxidative stress. In addition, oxidative stress may cause an increase in inflammation; however, the interactions between these factors are not fully understood. In this review, we propose the vascular health triad, which draws associations and interactions between oxidative stress and inflammation seen in ageing, and the consequences for vascular function. We review evidence suggesting that exercise may ameliorate the age-related decline in vascular function, through reductions in both oxidative stress and inflammation. Keywords Reactive oxygen and nitrogen species. Nitric oxide. Free radical. Inflammatory response. Older age. Endothelium Oxidative stress Reactive oxygen and nitrogen species (RONS) are highly reactive free radical species, characterised by the presence of one or more unpaired electrons in their

Plasma amino acid levels were measured in autistic and Asperger syndrome patients, their siblings, and parents. The results were compared with values from age-matched controls. Patients with autism or Asperger syndrome and their siblings and parents all had raised glutamic acid, phenylalanine, asparagine, tyrosine, alanine, and lysine (p < .05) than controls, with reduced plasma glutamine. Other amino acids were at normal levels. These results show that children with autistic spectrum disorders come from a family background of dysregulated amino acid metabolism and provide further evidence for an underlying biochemical basis for the condition.

Background In Mediterranean countries, adherence to a traditional Mediterranean dietary pattern (MedDiet) is associated with better cognitive function and reduced dementia risk. It is unclear if similar benefits exist in non-Mediterranean regions. Objectives The aims of this study were to examine associations between MedDiet adherence and cognitive function in an older UK population and to investigate whether associations differed between individuals with high compared with low cardiovascular disease (CVD) risk. Methods We conducted an analysis in 8009 older individuals with dietary data at Health Check 1 (1993–1997) and cognitive function data at Health Check 3 (2006–2011) of the European Prospective Investigation into Cancer and Nutrition–Norfolk (EPIC-Norfolk). Associations were explored between MedDiet adherence and global and domain-specific cognitive test scores and risk of poor cognitive performance in the entire cohort, and when stratified according to CVD risk status. Results Higher MedDiet adherence defined by the Pyramid MedDiet score was associated with better global cognition (β ± SE = −0.012 ± 0.002; P &lt; 0.001), verbal episodic memory (β ± SE = −0.009 ± 0.002; P &lt; 0.001), and simple processing speed (β ± SE = −0.002 ± 0.001; P = 0.013). Lower risk of poor verbal episodic memory (OR: 0.784; 95% CI: 0.641, 0.959; P = 0.018), complex processing speed (OR: 0.739; 95% CI: 0.601, 0.907; P = 0.004), and prospective memory (OR: 0.841; 95% CI: 0.724, 0.977; P = 0.023) was also observed for the highest compared with the lowest Pyramid MedDiet tertiles. The effect of a 1-point increase in Pyramid score on global cognitive function was equivalent to 1.7 fewer years of cognitive aging. MedDiet adherence defined by the Mediterranean Diet Adherence Screener (MEDAS) score (mapped through the use of both binary and continuous scoring) showed similar, albeit less consistent, associations. In stratified analyses, associations were evident in individuals at higher CVD risk only (P &lt; 0.05). Conclusions Higher adherence to the MedDiet is associated with better cognitive function and lower risk of poor cognition in older UK adults. This evidence underpins the development of interventions to enhance MedDiet adherence, particularly in individuals at higher CVD risk, aiming to reduce the risk of age-related cognitive decline in non-Mediterranean populations.

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