ABSTRACT
OBJETIVO: El propósito de este estudio es investigar la evidencia científica sobre el efecto del ejercicio físico respecto al estado cognitivo y conductual como medida preventiva y terapéutica no farmacológica en la enfermedad de Alzheimer (EA). DISEÑO: Revisión sistemática Fuentes de datos: Pubmed, Science Direct, Medline y Scopus, con las palabras clave: Alzheimer, Exercise, Neuroimaging, MRI, PET y Physical Activity. Selección de artículos: Se incluyeron aquellos estudios en los que se evaluaba el efecto del ejercicio físico en la evolución de la EA y que además contenían pruebas de imagen (resonancia magnética nuclear o tomografía por emisión de positrones) con marcador Pittsburg Compound B (PiB) analizando la atrofia cerebral o el aumento del depósito de beta-Amiloide respectivamente. Se excluyeron aquellos estudios en otros tipos de demencia que no fueran la EA, los que no incluían pruebas de neuroimagen, los casos únicos y aquellos de lengua no inglesa. Para la extracción de datos se utilizó la escala de calidad PRISMA para la lectura crítica de los estudios. Los investigadores evaluaron de forma independiente los artículos y las discrepancias se resolvieron por consenso. RESULTADOS: Se identificaron 75 artículos, de los cuales 23 fueron finalmente incluidos en la revisión. Concusiones: La mayoría de los estudios incluidos no permiten conocer la repercusión del ejercicio físico a nivel cognitivo y sobre los cambios estructurales y funcionales cerebrales en pacientes con riesgo de desarrollar la EA o en pacientes que ya presentan la enfermedad. Sin poder descartase un posible efecto beneficioso, son necesarios más estudios con un mejor diseño y rigor metodológico que permitan un mejor conocimiento de esta asociación
OBJECTIVE: The objective of this review is to analyze through a the scientific evidence about the effects of physical activity in patients with Alzheimer's disease (AD) as a preventive and non-pharmacological treatment. DESIGN: Systematic review. Data sources: We have identified articles from Pubmed, Science Direct, Medline and Scopus databases, with the keywords Alzheimer, Exercise, Neuroimaging, MRI, PET y Physical Activity. Selected articles: We included those studies that evaluated the effects of physical activity on Alzheimer's disease and those which also included magnetic resonance imaging or positron emission tomography with Pittsburg Compound B marker (PiB) analyzing brain atrophy or increase of the beta-amyloid deposit respectively. We excluded studies including other types of dementia, different of AD. We also excluded articles which not included neuroimaging tests, single cases or non-English language articles. Data extraction: The PRISMA quality scale was used for the critical lecture of the studies. The researchers independently assessed the articles and the discrepancies were resolved by consensus. RESULTS: We identified 75 articles, of which 23 were finally included in the review. CONCLUSIONS: Most of the studies included do not allow us to know the impact of physical exercise on cognition and the cerebral structural-functional changes in patients at risk of developing AD or in patients who already have the disease. Without being able to rule out a possible beneficial effect, more studies are needed with a better design and methodological rigor that allows a better known about this association
Subject(s)
Humans , Alzheimer Disease/therapy , Exercise Therapy , Alzheimer Disease/prevention & control , Exercise/physiology , Alzheimer Disease/diagnostic imaging , Positron Emission Tomography Computed Tomography , Magnetic Resonance SpectroscopyABSTRACT
OBJECTIVE: The objective of this review is to analyze through a the scientific evidence about the effects of physical activity in patients with Alzheimer's disease (AD) as a preventive and non-pharmacological treatment. DESIGN: Systematic review. DATA SOURCES: We have identified articles from Pubmed, Science Direct, Medline and Scopus databases, with the keywords Alzheimer, Exercise, Neuroimaging, MRI, PET y Physical Activity. Selected articles: We included those studies that evaluated the effects of physical activity on Alzheimer's disease and those which also included magnetic resonance imaging or positron emission tomography with Pittsburg Compound B marker (PiB) analyzing brain atrophy or increase of the beta-amyloid deposit respectively. We excluded studies including other types of dementia, different of AD. We also excluded articles which not included neuroimaging tests, single cases or non-English language articles. DATA EXTRACTION: The PRISMA quality scale was used for the critical lecture of the studies. The researchers independently assessed the articles and the discrepancies were resolved by consensus. RESULTS: We identified 75 articles, of which 23 were finally included in the review. CONCLUSIONS: Most of the studies included do not allow us to know the impact of physical exercise on cognition and the cerebral structural-functional changes in patients at risk of developing AD or in patients who already have the disease. Without being able to rule out a possible beneficial effect, more studies are needed with a better design and methodological rigor that allows a better known about this association.
Subject(s)
Alzheimer Disease/therapy , Exercise , Alzheimer Disease/diagnostic imaging , Alzheimer Disease/prevention & control , Amyloid beta-Peptides , Atrophy/diagnostic imaging , Brain/diagnostic imaging , Brain/pathology , Humans , Magnetic Resonance Imaging , Neuroimaging/methods , Positron-Emission TomographyABSTRACT
To assess the possible function of glutamate in the interaction between the dorsomedial hypothalamic nucleus-perifornical area (DMH-PeF) and the A5 pontine region (A5), cardiovascular and respiratory changes were studied in response to electrical stimulation of the DMH-PeF (1 ms pulses, 30-50 miA given at 100 Hz for 5 s) before and after the microinjection of kynurenic acid (non-specific glutamate receptor antagonist; 50 nl, 5 nmol), MK-801 (NMDA receptor antagonist; 50 nl, 50 nmol), CNQX (non-NMDA receptor antagonist; 50 nl, 50 nmol) or MCPG (metabotropic glutamate receptor antagonist; 50 nl, 5 nmol) within the A5 region. DMH-PeF electrical stimulation elicited a pressor (p < 0.001) and tachycardic response (p < 0.001) which was accompanied by an inspiratory facilitation characterised by an increase in respiratory rate (p < 0.001) due to a decrease in expiratory time (p < 0.01). Kynurenic acid within the A5 region decreased the tachycardia (p < 0.001) and the intensity of the blood pressure response (p < 0.001) to DMH-PeF stimulation. After the microinjection of MK-801 and CNQX into the A5 region, the magnitude of the tachycardia and the pressor response were decreased (p < 0.05 and p < 0.01; p < 0.001 and p < 0.05, respectively). After MCPG microinjection into the A5 region, a decrease in the tachycardia (p < 0.001) with no changes in the pressor response was observed during DMH-PeF stimulation. The respiratory response elicited by DMH-PeF stimulation was not changed after the microinjection of kynurenic acid, MK-801, CNQX or MCPG within the A5 region. These results suggest that A5 region glutamate receptors play a role in the cardiovascular response elicited from the DMH-PeF. The possible mechanisms involved in these interactions are discussed