Effect of exercise on cognitive function and synaptic plasticity in Alzheimer's disease models: A systematic review and meta-analysis

Abstract

IntroductionCognitive decline is a central manifestation of Alzheimer's disease (AD), and its process is inseparable from changes in synaptic plasticity. The aim of this review was to summarize and evaluate the effectiveness of exercise on cognitive function and synaptic plasticity in AD animal models.Materials and methodsEligible studies were searched from PubMed, MEDLINE, EMBASE, Web of Science, and Cochrane Library from April to May 2022. The risk of bias was evaluated by Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE). The Morris water maze (MWM) test and synaptic plasticity were considered outcome measures. Data were analyzed using random-effects meta-analyses using the software Stata. Heterogeneity was examined by using I2 test. Sensitivity analysis and publication bias were also assessed.ResultsA total of 20 randomized controlled studies were eligible for study inclusion. Compared with controls, exercise decreased escape latency (SMD = −0.86, 95% CI: −1.21 to −0.50, P < 0.001), increased platform crossover numbers (SMD = 1.34, 95% CI: 0.57–2.11, P = 0.001) and time in the target quadrant (SMD = 1.65, 95% CI: 0.95–2.36, P < 0.001) and the expression of PSD95 (SMD = 0.73, 95% CI: 0.25–1.21, P = 0.003) in AD animals. The results of the subgroup analysis showed that exercise before AD had a greater effect on escape latency (SMD = −0.88, 95% CI: −1.25 to −0.52, P < 0.001), platform crossover numbers (SMD = 1.71, 95% CI: 1.23–2.18, P < 0.001), time in the target quadrant (SMD = 2.03, 95% CI: 1.19–2.87, P < 0.001) and the expression of PSD95 (SMD = 0.94, 95% CI: 0.19–1.69, P = 0.014) than exercise after AD. The results of the subgroup analysis also showed that treadmill running might be an appropriate exercise type.ConclusionOur findings suggested that exercise had a potential effect on improving cognitive function and synaptic plasticity. It can play a better neuroprotective role before AD.Systematic review registrationPROSPERO, identifier: CRD42022328438.

Early Detection of Alzheimer’s Disease in Postmenopausal Women Using Thalamic Subnuclear Volumetry

“…The neuropathological hallmarks of AD include "positive" lesions, such as amyloid plaques, cerebral amyloid angiopathy, neurofibrillary tangles, and glial responses, and "negative" lesions, such as neuronal and synaptic loss [5][6][7][8][9]. Among the neuropathological alterations in AD, relevant neuronal loss and synaptic pathology have been directly associated with the severity of cognitive dysfunction in patients with AD [10,11].…”

Terminally differentiated effector memory T cells associate with cognitive and AD-related biomarkers in an aging-based community cohort

“…The innate and adaptive immune system, essential for protecting individuals against infections, injury, and diseases, is profoundly impacted by chronological aging, becoming less protective and more inflammatory [1] . The age-associated decline in T cell function contributes to increased susceptibility to infections such as influenza, COVID-19, pneumonia, and urinary tract infections (UTI) [1,2] . Beyond aging, changes in adaptive immune responses are exacerbated in Alzheimer's disease and related dementias (ADRD) [3][4][5][6][7][8][9][10] .…”