Evaluation of the cerebral vascular morphostructural in a model for Alzheimer’s disease after the intervention with physical exercise.

Abstract

AbstractBackgroundAlzheimer’s disease (AD) is the most common neurodegenerative disease in the world. It is characterized by impaired memory, thinking, orientation, and learning, thus affecting the quality of life of people whosuffer from it. The two pathognomonic hallmarks are the neuritic plaques and neurofibrillary tangles, however, the vascular system is also affected, aggravating the symptoms of the disease, being a possible hypothesis of the development of the disease. One of the most widely used animal models to study disease mechanisms is the 3xTg‐AD triple transgenic mouse that contains three mutations associated with familial AD (PS1M146V, APPSWE, and tauP301L). Among the non‐pharmacological treatments is physical exercise, which is a variety of planned, repetitive, and dosed physical activity, proving to be safe as part of the adjuvant treatment of the disease, however, its effect on the vascular system is unknown.MethodA total of 40 ten‐month‐old female mice, 3xTg‐AD (n = 20) and NonTg (n = 20), equally divided into exercise and sedentary groups, were used. An intervention of voluntary physical exercise was carried out for 3 months with a frequency of 5 times a week. Subsequently, memory and learning were evaluated using the Barnes maze test. The vascular morphostructure by anatomical analysis through histological assays using markers for vascular basement membrane (anti‐Collagen IV) and pericytes (anti‐PDGFR‐β), in addition to amyloid deposits. No improvement in cognitive ability was observed, however, exercise promoted the recovery of the vascular system, as well as the reduction of amyloid deposits.ResultNo improvement in cognitive ability was observed, however, exercise promoted the recovery of the vascular system, as well as the reduction of amyloid deposits.ConclusionThe intervention with voluntary physical exercise promotes stability of the vascular system as well as the reduction of amyloid deposits in the symptomatic stages of the disease.