Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-βpeptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented.

Serotonin is an ancient molecular signal and a recognized neurotransmitter brainwide distributed with particular presence in hippocampus. Almost all serotonin receptor subtypes are expressed in hippocampus, which implicates an intricate modulating system, considering that they can be localized as autosynaptic, presynaptic, and postsynaptic receptors, even colocalized within the same cell and being target of homo- and heterodimerization. Neurons and glia, including immune cells, integrate a functional network that uses several serotonin receptors to regulate their roles in this particular part of the limbic system.

Background: Major depressive disorders are characterized by their severity and long‐lasting symptoms, which make such disorders highly disabling illnesses. Unfortunately, 50% of major depressive patients experience relapses, perhaps partly because drug research has been performed only in animal models that screen for antidepressant drugs that appear to only ameliorate acute depression symptoms. The bilateral olfactory bulbectomy (OBX) animal model presents the advantage of mimicking the symptoms of chronic depression by means of brain surgery. Adenosine purinergic receptors A2A (A2AR) have been the target of interest in the field of psychiatric diseases. This study aimed to show which A2A receptor ligands exert antidepressive‐like effects in the OBX rat model.Methods: Forty Sprague‐Dawley male rats were divided into four groups: control, OBX + vehicle, OBX + ZM 241385, and OBX + adenosine groups. Pharmacological treatment was administered for 14 days, and the rats were examined via the forced swim test (FST), open field test (OFT), and sucrose preference test (SPT).Results: The OBX + ZM 241385 group exhibited decreased immobility time in the FST, decreased isolation time in the OFT, and reversed anhedonia behavior in the SPT compared to the vehicle group. However, no significant differences for adenosine treatment were found.Conclusions: ZM 241385 administration (2 mg/kg i.p.) restored behavioral changes associated with OBX‐induced depression.

It is known that serotonin exerts its different nociceptive and motor functions by interacting with distinct receptors subtypes, which could be either G-protein coupled or ionotropic. Previous reports demonstrated the early activation of serotonin receptor transcripts during rat development, suggesting a potential role of the serotoninergic system during ontogeny. In this study we have compared the cellular distribution of three serotonin receptor subtypes: 5-HT_2C, 5-HT_5A, and 5-HT₇. Immunocytochemical methods were used in slices of rat hippocampus obtained during the postnatal development. 5-HT_2C immunoreactivity was strong at all developmental stages in the CA1 region, whereas differences were observed between P0 and P5 in the CA3 region. The 5-HT_5A receptor immunosignal in CA1 and CA3 was strong at P0, decreased at P11, and then increased in the adult. The immunoreactivity to 5-HT₇ receptors was high in all regions at P0 and then decreased progressively during postnatal development; the signal was stronger for 5-HT_2C than for 5-HT_5A and 5-HT₇ receptors. Changes in the expression level of each receptor may result in differences in functional and pharmacological properties of the cells expressing them as well as in the hippocampal neuronal network. The distribution of the three serotonin receptor subtypes studied varied during the ontogeny, which supports their potential role during development and will help to understand their mechanisms.