While the relationship between increased physical activity and cognitive ability has been conjectured for centuries, only recently have the mechanisms underlying this relationship began to emerge. Convergent evidence suggests that physical activity offers an affordable and effective method to improve cognitive function in all ages, particularly the elderly who are most vulnerable to neurodegenerative disorders. In addition to improving cardiac and immune function, physical activity alters trophic factor signaling and, in turn, neuronal function and structure in areas critical for cognition. Sustained exercise plays a role in modulating anti-inflammatory effects and may play a role in preserving cognitive function in aging and neuropathological conditions. Moreover, recent evidence suggests that myokines released by exercising muscles affect the expression of brain-derived neurotrophic factor synthesis in the dentate gyrus of the hippocampus, a finding that could lead to the identification of new and therapeutically important mediating factors. Given the growing number of individuals with cognitive impairments worldwide, a better understanding of how these factors contribute to cognition is imperative, and constitutes an important first step toward developing non-pharmacological therapeutic strategies to improve cognition in vulnerable populations.

Alzheimer disease (AD) is a primary cause of cognitive dysfunction in the elderly population worldwide. Despite the allocation of enormous amounts of funding and resources to studying this brain disorder, there are no effective pharmacological treatments for reducing the severity of pathology and restoring cognitive function in affected people. Recent reports on the failure of multiple clinical trials for AD have highlighted the need to diversify further the search for new therapeutic strategies for cognitive dysfunction. Thus, studies detailing the neuroprotective effects of physical activity (PA) on the brain in AD were reviewed, and mechanisms by which PA might mitigate AD-related cognitive decline were explored. A MEDLINE database search was used to generate a list of studies conducted between January 2007 and September 2014 (n=394). These studies, along with key references, were screened to identify those that assessed the effects of PA on AD-related biomarkers and cognitive function. The search was not limited on the basis of intensity, frequency, duration, or mode of activity. However, studies in which PA was combined with another intervention (eg, diet, pharmacotherapeutics, ovariectomy, cognitive training, behavioral therapy), and studies not written in English were excluded. Thirty-eight animal and human studies met entry criteria. Most of the studies suggested that PA attenuates neuropathology and positively affects cognitive function in AD. Although the literature lacked sufficient evidence to support precise PA guidelines, convergent evidence does suggest that the incorporation of regular PA into daily routines mitigates AD-related symptoms, especially when deployed earlier in the disease process. Here the protocols used to alter the progression of AD-related neuropathology and cognitive decline are highlighted, and the implications for physical therapist practice are discussed.

While it has been known that physical activity can improve cognitive function and protect against neurodegeneration, the underlying mechanisms for these protective effects are yet to be fully elucidated. There is a large body of evidence indicating that physical exercise improves neurogenesis and maintenance of neurons. Yet, its possible effects on glial cells remain poorly understood. Here, we tested whether physical exercise in mice alters the expression of trophic factor-related genes and the status of astrocytes in the dentate gyrus of the hippocampus. In addition to a significant increase in Bdnf mRNA and protein levels, we found that 4 weeks of treadmill and running wheel exercise in mice, led to (1) a significant increase in synaptic load in the dentate gyrus, (2) alterations in astrocytic morphology, and (3) orientation of astrocytic projections towards dentate granule cells. Importantly, these changes were possibly linked to increased TrkB receptor levels in astrocytes. Our study suggests that astrocytes actively respond and could indeed mediate the positive effects of physical exercise on the central nervous system and potentially counter degenerative processes during aging and neurodegenerative disorders.

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Dendritic arborization has been shown to be a reliable marker for examination of structural and functional integrity of neurons. Indeed, the complexity and extent of dendritic arborization correlates well with the synaptic plasticity in these cells. A reliable method for assessment of dendritic arborization is needed to characterize the deleterious effects of neurological disorders on these structures and to determine the effects of therapeutic interventions. However, quantification of these structures has proven to be a formidable task given their complex and dynamic nature. Fortunately, sophisticated imaging techniques can be paired with conventional staining methods to assess the state of dendritic arborization, providing a more reliable and expeditious means of assessment. Below is an example of how these imaging techniques were paired with staining methods to characterize the dendritic arborization in wild type mice. These complementary imaging methods can be used to qualitatively and quantitatively assess dendritic arborization that span a rather wide area within the hippocampal region.

Context. Recent studies have demonstrated a strong association between cardiorespiratory fitness (CRF) and mortality, but bias due to differences in the distribution of baseline variables has not been adequately considered. We studied a cohort of veterans with and without Type-2 diabetes using a propensity score matching method. Methods. Males with (n=592) and without (n= 6,167) Type-2 diabetes were studied. Propensity scores were used to balance covariate distributions between groups with and without Type-2 diabetes. All-cause mortality was the end point. Results. Predictors of mortality included hypertension, smoking, Type-2 diabetes, BMI and CRF. For each 1 MET increase in CRF in the unmatched group, the adjusted HR was 0.83 in those with diabetes (95% CI 0.77-0.89; p<0.0001) compared to 0.87 in those without diabetes (95% CI 0.86-0.89; p<0.0001). Similar trends were observed for the matched dataset: the adjusted HRs were 0.83 (95% CI 0.77-0.90; p<0.0001) and 0.88 (95% CI 0.82-0.94; p<0.0001) for those with and without diabetes, respectively. Conclusions. CRF is a strong predictor of mortality in veterans with and without Type-2 diabetes. Although the trend in the association between CRF and all-cause-mortality was similar for matched and unmatched data, the mortality risks were relatively inflated when using unmatched data.

Presentación de casos clínicos RESUMEN La anafilaxia es una reacción de hipersensibilidad sistémica y grave, de inicio rápido y potencialmente mortal. En los recién nacidos prematuros, el sistema inmunitario aún no ha madurado y, por lo tanto, tienen menos probabilidades de presentar anafilaxia. La administración de amikacina, que contenía metabisulfito de sodio, a un prematuro de 3 días de vida le indujo anafilaxia casi mortal. Debido a que se sospechaba un caso de anafilaxia, se inició la administración de amikacina en el bebé. Una vez comenzado el tratamiento, se observó una mejoría clínica. Al tercer día de tratamiento con amikacina, el recién nacido tuvo, repentinamente, taquipnea, taquicardia, angioedema y cianosis. Se le diagnosticó anafilaxia y se inició el tratamiento. Una hora después de la mejoría clínica, se produjo una reacción tardía. Inmediatamente, se intubó al recién nacido. La anafilaxia es una emergencia médica; por lo tanto, los médicos deben realizar una evaluación rápida y atenta para detectar esta reacción potencialmente mortal. Incluso después del tratamiento satisfactorio de la anafilaxia, el paciente debe permanecer bajo observación durante 72 horas dada la posibilidad de una reacción bifásica.