Abstract
PurposeVascular dysfunction has been demonstrated in patients with Alzheimer’s disease (AD). Exercise is known to positively affect vascular function. Thus, the aim of our study was to investigate exercise-induced effects on vascular function in AD.MethodsThirty-nine patients with AD (79 ± 8 years) were recruited and randomly assigned to exercise training (EX, n = 20) or control group (CTRL, n = 19). All subjects performed 72 treatment sessions (90 min, 3 t/w). EX included moderate–high-intensity aerobic and strength training. CTRL included cognitive stimuli (visual, verbal, auditive). Before and after the 6-month treatment, the vascular function was measured by passive-leg movement test (PLM, calculating the variation in blood flow: ∆peak; and area under the curve: AUC) tests, and flow-mediated dilation (FMD, %). A blood sample was analyzed for vascular endothelial growth factor (VEGF). Arterial blood flow (BF) and shear rate (SR) were measured during EX and CTRL during a typical treatment session.ResultsEX group has increased FMD% (+ 3.725%, p < 0.001), PLM ∆peak (+ 99.056 ml/min, p = 0.004), AUC (+ 37.359AU, p = 0.037) and VEGF (+ 8.825 pg/ml, p = 0.004). In the CTRL group, no difference between pre- and post-treatment was found for any variable. Increase in BF and SR was demonstrated during EX (BF + 123%, p < 0.05; SR + 134%, p < 0.05), but not during CTRL treatment.ConclusionExercise training improves peripheral vascular function in AD. These ameliorations may be due to the repetitive increase in SR during exercise which triggers NO and VEGF upregulation. This approach might be included in standard AD clinical practice as an effective strategy to treat vascular dysfunction in this population.
Highlights
Alzheimer’s disease (AD) is one of the most common agerelated diseases (Alzheimer’s Association 2019), mainly known for its cognitive symptoms that interfere with activities of daily life and impact memory loss, learning, language, and behavior (Alzheimer’s Association 2019; Rhodin and Thomas 2001)
Despite decades of investigations focused on understanding the mechanisms that cause these changes in the brain in AD, to date, there is no treatment for AD, and no interventions to delay or prevent AD, or to alleviate symptoms and comorbidities (Dede et al 2007; Barnes and Corkery 2018; Rhodin and Thomas 2001)
Several recent studies explored mechanisms different from Aβ plaque deposition and neurofibrillary tangles that may be involved in AD onset and development (Rhodin and Thomas 2001; Barnes and Corkery 2018; Eldholm et al 2018; Sweeney et al 2019; Pedrinolla et al 2017; Venturelli et al 2018)
Summary
Alzheimer’s disease (AD) is one of the most common agerelated diseases (Alzheimer’s Association 2019), mainly known for its cognitive symptoms that interfere with activities of daily life and impact memory loss, learning, language, and behavior (Alzheimer’s Association 2019; Rhodin and Thomas 2001). Focal constriction, reduced perfusion of the temporal and frontal cortices, structural changes in endothelial cells, Aβ deposition in vessel walls are some of the vascular changes that have been reported in individuals with AD Based on these findings, it has been hypothesized that the primary site of the onset of AD, and the target of the toxic Aβ are vessels, small arteries, arterioles, and capillaries of the central nervous system (Rhodin and Thomas 2001; Dede et al 2007; Venturelli et al 2018). Extracranial and peripheral vascular dysfunction appeared to have a linear relationship with cognitive dysfunction (Venturelli et al 2018) suggesting that vascular function (both central and peripheral) may play a key role in AD
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