Publications by authors named "Ines Marques-Aleixo"

Background: Neuropsychiatric symptoms (NPS) are highly prevalent among individuals with major neurocognitive disorders (MNCD).

Objective: Here, we characterized blood biomarkers (metabolic, inflammatory, neurotrophic profiles and total antioxidant), body composition, physical fitness and quality of life (QoL) in individuals with MNCD according to NPS.

Methods: The sample comprised 34 older adults (71.

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Sarcopenia is a well-known highly prevalent muscle disease that severely impairs overall physical performance in elders, inducing a massive health-related economic burden. The widespread screening, diagnosis and treatment of sarcopenia are pivotal to restrain the disease progression and constrain its societal impact. Simple-to-use, portable, and reliable methods to evaluate sarcopenia are scarce, and sarcopenia-related assessments are typically done in several time-consuming stages.

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The availability of wearable devices (WDs) to collect biometric information and their use during activities of daily living is significantly increasing in the general population. These small electronic devices, which record fitness and health-related outcomes, have been broadly utilized in industries such as medicine, healthcare, and fitness. Since they are simple to use and progressively cheaper, they have also been used for numerous research purposes.

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Article Synopsis
  • Dementia is a significant health challenge and regular physical activity, particularly Multicomponent Training (MT), is being studied as a way to improve physical and cognitive function in individuals with dementia.
  • The "Body & Brain" study will assess the effects of a 6-month MT program followed by a 3-month period without exercise, focusing on physical, cognitive, psychosocial factors, and physiological markers.
  • Participants aged 60 and over will be split into an intervention group that engages in biweekly MT sessions and a control group receiving monthly information sessions on health, with various outcomes measured throughout the study.
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The prevalence and incidence of age-related neurodegenerative diseases (NDDs) tend to increase along with the enhanced average of the world life expectancy. NDDs are a major cause of morbidity and disability, affecting the health care, social and economic systems with a significant impact. Despite the worldwide burden of NDDs and the ongoing research efforts to increase the underlying molecular mechanisms involved in NDD pathophysiologies, pharmacological therapies have been presenting merely narrow benefits.

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Doxorubicin (DOX), a widely used and efficient antineoplastic agent, is mainly limited by cardiotoxicity, although other tissues including liver are also affected. The effects of exercise to cope with DOX side-effects has already been studied in the heart and brain, demonstrating successful results. However, the benefits of this non-pharmacological strategy have not been so extensively checked in the liver.

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This quasi-experimental, nonrandomized study examined the feasibility and impact of a multicomponent (MT) intervention on 7 community-dwelling individuals diagnosed with probable Alzheimer's disease (AD) at mild to moderate stage. During 6 months, patients with AD and their caregivers were submitted to a biweekly exercise program, including muscle strengthening, aerobics, balance, and postural exercises. The following tests were used: Senior Fitness Test and Incremental Treadmill Test, Disability Assessment for Dementia Scale, Alzheimer Disease Assessment Scale-Cognitive, and Quality of Life-Alzheimer's.

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Doxorubicin (DOX) is an anti-cancer agent whose clinical usage results in a cumulative and dose-dependent cardiotoxicity. We have previously shown that exercise performed prior to DOX treatment reduces the resulting cardiac(mito) toxicity. We sought to determine the effects on cardiac mitochondrial toxicity of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free-wheel activity-FW) when used prior and during DOX treatment.

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Background: Several strategies have been developed to counteract liver injury as a consequence of nonsteroid anti-inflammatory drugs toxicity. Here, we aimed to determine whether physical exercise results in liver mitochondrial protection against in vitro diclofenac toxicity.

Material And Methods: Male adult Sprague-Dawley rats were divided into sedentary, 12-week endurance training (ET) and voluntary activity (VPA).

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Exercise is considered a non-pharmacological tool against several lifestyle disorders in which mitochondrial dysfunction is involved. The present study aimed to analyze the preventive (voluntary physical activity-VPA) and therapeutic (endurance training-ET) role of exercise against non-alcoholic steatohepatitis (NASH)-induced liver mitochondrial dysfunction. Sixty male Sprague-Dawley rats were divided into standard-diet sedentary (SS, n=20), standard-diet VPA (SVPA, n=10), high-fat diet sedentary (HS, n=20) and high-fat diet VPA (HVPA, n=10).

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Aims: Aging and drug-induced side effects may contribute to deteriorate mitochondrial bioenergetics in many tissues, including kidney and liver. One possibility is that the combination of both aging and drug toxicity accelerates the process of mitochondrial degradation, leading to progressive bioenergetic disruption. We therefore analyzed in vitro kidney (KM) and liver (LM) mitochondrial response to salicylate and diclofenac in old and adult animals.

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This study examined the differences in intracycle velocity variation and arm coordination in front crawl in swimmers with Down syndrome in three breathing conditions. International swimmers with Down syndrome (N = 16) performed 3 × 20 m front crawl at 50 m race speed: without breathing, breathing to the preferred side, and breathing to the nonpreferred side. A two dimensional video movement analysis was performed using the APASystem.

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Aging and neurodegenerative conditions such as Alzheimer and Parkinson diseases are characterized by tissue and mitochondrial changes that compromise brain function. Alterations can include increased reactive oxygen species production and impaired antioxidant capacity with a consequent increase in oxidative damage, mitochondrial dysfunction that compromises brain ATP production, and ultimately increased apoptotic signaling and neuronal death. Among several non-pharmacological strategies to prevent brain degeneration, physical exercise is a surprisingly effective strategy, which antagonizes brain tissue and mitochondrial dysfunction.

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