So .You Want to be a Peer Reviewer?

Peer review is essential to preserving the integrity of the scientific publication process. Peer reviewers must adhere to the norms of the peer review process, including confidentiality, avoiding actual or apparent conflicts of interest, timeliness, constructiveness, and thoroughness. This mini review will discuss some of the different formats in which peer review might occur, as well as advantages and disadvantages of each. The topics then shift to providing advice for prospective reviewers, as well as a suggested format for use in writing a review.

An Update on Sphingosine-1-Phosphate and Lysophosphatidic Acid Receptor Transcripts in Rodent Olfactory Mucosa.

Olfactory neurons connect the external environment and the brain, allowing the translocation of materials from the nasal cavity into the brain. The olfactory system is involved in SARS-CoV-2 infections; early in the pandemic declared in 2020, a loss of the sense of smell was found in many infected patients. Attention has also been focused on the role that the olfactory epithelium appears to play in the entry of the SARS-CoV-2 virus into the brain. Specifically, SARS-CoV-2 enters cells via the angiotensin-converting enzyme 2 protein (ACE2), which is found on supporting cells in the olfactory epithelium. The intranasal administration of sphingosine has been proposed to prevent the binding of SARS-CoV-2 to ACE2. Further, sphingosine-1-phosphate (S1P) receptors appear to facilitate the entry of SARS-CoV-2 into the brain. The goal of these studies was to characterize S1P receptor expression status in rodent olfactory mucosa. The expression of receptors for a related sphingolipid, lysophosphatidic acid (LPA), was also assessed. The results confirm previous reports of S1P1 and S1P3 receptor expression, as well as LPA receptor 1, in mouse olfactory mucosa; moreover, they extend the previous findings to identify additional S1P and LPA receptor transcripts in rat and mouse olfactory mucosa, as well as in cultured olfactory neurons. These findings may enhance the utility of rodent models in identifying agonists and/or antagonists of S1P and LPA receptors that may block the entry of SARS-CoV-2 and other viruses into nasal epithelial cells, and prevent transmission from the nasal cavity into the brain.

Intranasal Carnosine Mitigates α-Synuclein Pathology and Motor Dysfunction in the Thy1-aSyn Mouse Model of Parkinson's Disease.

Parkinson's disease (PD) is a debilitating neurodegenerative disorder. Early symptoms include motor dysfunction and impaired olfaction. Toxic aggregation of α-synuclein (aSyn) in the olfactory bulb (OB) and substantia nigra pars compacta (SNpc) is a hallmark of PD neuropathology. Intranasal (IN) carnosine (2 mg/d for 8 weeks) was previously demonstrated to improve motor behavior and mitochondrial function in Thy1-aSyn mice, a model of PD. The present studies evaluated the efficacy of IN carnosine at a higher dose in slowing progression of motor deficits and aSyn accumulation in Thy1-aSyn mice. After baseline neurobehavioral assessments, IN carnosine was administered (0.0, 2.0, or 4.0 mg/day) to wild-type and Thy1-aSyn mice for 8 weeks. Olfactory and motor behavioral measurements were repeated prior to end point tissue collection. Brain sections were immunostained for aSyn and tyrosine hydroxylase (TH). Immunopositive cells were counted using design-based stereology in the SNpc and OB mitral cell layer (MCL). Behavioral assessments revealed a dose-dependent improvement in motor function with increasing carnosine dose. Thy1-aSyn mice treated with 2.0 or 4.0 mg/d IN carnosine exhibited fewer aSyn-positive (aSyn(+)) cell bodies in the SNpc compared to vehicle-treated mice. Moreover, the number of aSyn(+) cell bodies in carnosine-treated Thy1-aSyn mice was reduced to vehicle-treated wild-type levels in the SNpc. Carnosine treatment did not affect the number of aSyn(+) cell bodies in the OB-MCL or the number of TH(+) cells in the SNpc. In summary, intranasal carnosine treatment decreased aSyn accumulation in the SNpc, which may underlie its mitigation of motor deficits in the Thy1-aSyn mice.

Toxic exposures and the senses of taste and smell.

This review addresses the adverse influences of neurotoxic exposures on the ability to smell and taste. These chemical senses largely determine the flavor of foods and beverages, impact food intake, and ultimately nutrition, and provide a warning for spoiled or poisonous food, leaking natural gas, smoke, airborne pollutants, and other hazards. Hence, toxicants that damage these senses have a significant impact on everyday function. As noted in detail, a large number of toxicants encountered in urban and industrial air pollution, including smoke, solvents, metals, and particulate matter can alter the ability to smell. Their influence on taste, i.e., sweet, sour, bitter, salty, and savory (umami) sensations, is not well documented. Given the rather direct exposure of olfactory receptors to the outside environment, olfaction is particularly vulnerable to damage from toxicants. Some toxicants, such as nanoparticles, have the potential to damage not only the olfactory receptor cells, but also the central nervous system structures by their entrance into the brain through the olfactory mucosa.

Evaluation of Carnosine Intervention in the Thy1-aSyn Mouse Model of Parkinson's Disease.

Parkinson disease (PD) is a leading neurodegenerative disease, with multifaceted interacting mechanisms. The Thy1-aSyn mouse model of PD exhibits many features of PD patients, including sensorimotor and olfactory dysfunction and protein aggregation. Here, we tested the hypothesis that the dipeptide carnosine, which has anti-aggregating and metal-chelating properties, would provide beneficial effects on the motor and olfactory deficits observed in Thy1-aSyn mice. After 2 months of daily treatment with either intranasal (2 mg/day) or oral (10 mM in drinking water) carnosine, Thy1-aSyn mice and wild-type BDF1 mice were assessed for sensorimotor (challenging beam traversal test and spontaneous activity) and olfactory (buried pellet test) function. In addition, the olfactory epithelium was evaluated immunohistochemically for expression of alpha-synuclein (aSyn) and the carnosine transporter Pept2. Olfactory function was unaffected by carnosine treatment via either administration route. In contrast, intranasal carnosine prevented the normal decline in gait function seen in the challenging beam test in the Thy1-aSyn mice. Moreover, carnosine-treated Thy1-aSyn mice exhibited decreased aSyn immunostaining in the olfactory epithelium compared to vehicle-treated Thy1-aSyn mice, and the carnosine transporter Pept2 was immunolocalized to the apical surface of the olfactory epithelium. These findings demonstrate that intranasal carnosine shows promise in slowing the progression of motor deficits and aSyn deposition in PD.