Effects of metformin on recognition memory and hippocampal neuroplasticity in rats with metabolic syndrome.
Guadalupe Muñoz-ArenasGuadalupe PulidoTreviño SamuelRubén Antonio Vázquez-RoqueGonzalo FloresCarolina MoránAnabella Handal-SilvaJorge GuevaraBerenice VenegasAlfonso Diaz-FonsecaePublished in: Synapse (New York, N.Y.) (2020)
Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first-line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90-day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin-1, AMP-activated protein kinase, and brain-derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.
Keyphrases
- mass spectrometry
- metabolic syndrome
- multiple sclerosis
- ms ms
- cerebral ischemia
- working memory
- protein kinase
- healthcare
- public health
- blood pressure
- brain injury
- white matter
- cardiovascular disease
- type diabetes
- uric acid
- emergency department
- cardiovascular risk factors
- subarachnoid hemorrhage
- drug induced
- adverse drug
- resting state
- functional connectivity
- skeletal muscle
- risk assessment
- smoking cessation
- arterial hypertension