Anosmia or Ageusia Following COVID-19 Vaccination: A Systematic Review.

Aim: To systematically review the cases of anosmia or ageusia after receiving the coronavirus disease 2019 (COVID-19) vaccine. Methods: A systematic search was conducted in electronic databases, including Web of Science, Scopus, Embase, and PubMed, to identify any published study that evaluated the anosmia or ageusia after receiving the COVID-19 vaccine, including case reports, case series, letter to editor articles with reported cases regarding our topic, or observational studies with at least 1 eligible patient consisted with our criteria. We excluded the studies that reported anosmia or ageusia due to COVID-19 infection and non-COVID-19 vaccines. Results: Five studies consisting of 11 patients were included in this systematic review. Of the 11 patients, 5 patients had received the Pfizer COVID-19 vaccine and 6 patients received the Oxford-AstraZeneca COVID-19 vaccine, of which 6 patients developed symptoms after the first dose of vaccination and 5 patients were symptomatic after the second vaccine dose. Most of the patients developed symptoms within 1 week after the vaccination. The disorders of the patients included partial or total anosmia, parosmia, phantosmia, hyposmia, ageusia, and dysgeusia. Also, the patients had symptoms other than smell or taste disorders, including arthralgia, fever, chills, rhinorrhea, myalgia, abdominal pain, fatigue, muscle weakness, altered bowel pattern, aural fullness, tinnitus, and headache. Most of the evaluated patients did not receive any treatment as for their disorders. However, in some cases, treatment with oral corticosteroids or dietary supplementation was required. Conclusion: Anosmia and ageusia are important symptoms of COVID-19 vaccination. These symptoms will resolve without any treatment in most cases, although some interventions may be needed in some patients.

Olfaction alters spatial memory strategy of scatter-hoarding animals.

Although it has been suggested that olfaction is closely interconnected with hippocampal systems, whether olfaction regulates spatial memory strategy remains never known. Furthermore, no study has examined how olfaction mediates spatial memory established on the external objects, for example, caches made by scatter-hoarding animals. Here, we experimentally induced nondestructive and reversible olfaction loss of a scatter-hoarding animal Leopoldamys edwardsi, to test whether and how olfaction regulates spatial memory to mediate cache recovery and pilferage. Our results showed that the normal L. edwardsi preferred to pilfer caches of others rather than to recover their own using accurate spatial memory (35.7% vs. 18.6%). Anosmic L. edwardsi preferred to recover the caches they made prior to olfaction loss rather than to pilfer from others relied on spatial memory (54.2% vs. 36.0%). However, L. edwardsi with anosmia showed no preference either to the caches they established after olfaction loss or caches made by others (25.8% vs. 29.1%). These collectively indicate that olfaction loss has a potential to affect new memory formation but not previously established spatial memory on caches. Our study first showed that olfaction modified spatial memory strategy in cache recovery and pilferage behaviors of scatter-hoarding animals. We suggest that future studies pay more attention to the evolution of olfaction and its relationship with spatial memory strategy.

Type 3 adenylyl cyclase in the MOE is involved in learning and memory in mice.

Although olfactory dysfunction is related to learning and memory impairment, the causal relationship between main olfactory epithelium (MOE) disruption and learning and memory is still unknown. The present study aimed to establish whether MOE disruption causes learning and memory impairment and whether the expression of type 3 adenylyl cyclas (AC3) in the MOE is related to learning and memory. First, the buried food test was carried out to confirm that MOE function was disrupted in mice treated with nasal instillation of zinc sulfate (ZnSO4 mice), and mice with specific knockdown of AC3 in the MOE by CRISPR/Cas9 technology (AC3KD/MOE mice). Then, behavioural tasks associated with learning and memory were administered. ZnSO4 mice and AC3KD/MOE mice showed impairments in learning and memory tests, including the novel object recognition test, the step-down passive avoidance test, the Morris water maze test, and the Y-maze test. Our data demonstrate that MOE disruption caused by nasal exposure to ZnSO4 or specific knockdown of AC3 in the MOE resulted in learning and memory impairment, and they further demonstrate that the expression of AC3 in the MOE plays a major role in learning and memory.

A single intranigral administration of ß-sitosterol ß-d-glucoside elicits bilateral sensorimotor and non-motor alterations in the rat.

Parkinson's disease (PD) is a progressive neuropathology characterized by motor and non-motor alterations. ß-sitosterol ß-d-glucoside (BSSG) is a neurotoxin whose prolonged oral administration in rats has been proposed as a new PD model. Herein, we demonstrate that a single, unilateral, and intranigral administration of BSSG also elicits bilateral sensorimotor alterations in the rat. Six behavioral tests evaluated the effect of different concentrations of BSSG (3, 6, 9, and 12 µg/µL DMSO) from 15 to 120 days after administration. The first behavioral alterations, which appeared on day 15, were unbalanced and uncoordinated gaits and a decrease in the sensorimotor cortex activity, as evidenced by the beam-walking and the vibrissae tests, respectively. After 30 days, the corridor test revealed hyposmia and a decreased locomotor activity in the open field. The last alteration was a depressive-like behavior, as shown by the forced swim test on days 60 and 120. According to the cylinder test, no locomotor asymmetry was observed over time with any BSSG concentrations tested. Also, a mesencephalic TH(+) cell loss (p < 0.05) was shown on day 30 when compared with the mock condition, and such a loss was even higher on day 120. At this time, the presence of pathological α-synuclein aggregates in the mesencephalon was documented. Our results show that the stereotaxic intranigral administration of BSSG reproduces some characteristics of oral administration, such as the progression of behavioral alterations, dopaminergic neurons loss, and the presence of Lewy body-like synuclein aggregations, in less time and resources.