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Brain Sciences Jul 2022The present study aimed to investigate the association between the functional connectivity (FC) of the olfactory cortex and olfactory performance in Parkinson's disease...
The present study aimed to investigate the association between the functional connectivity (FC) of the olfactory cortex and olfactory performance in Parkinson's disease (PD). Eighty-two early PD patients and twenty-one healthy controls underwent structural and resting-state functional MRI scans, as well as neuropsychological assessments from the Parkinson's Progression Markers Initiative database. A whole brain voxel-wise regression analysis was conducted to evaluate the relationship between the FC of the entorhinal cortex (EC-FC) and olfactory performance. Then, a one-way ANCOVA, based on the regions of interest, was performed with SPSS to investigate the group differences and correlation analysis that were used to analyze the relationships between the FC and neuropsychological assessments. In addition, regression models were used to evaluate the risk factors for the decreased olfactory function. A significantly negative correlation was observed between the olfactory performance and the left EC-FC in the right dorsal cingulate gyrus (dCC) in patients. The PD patients with anosmia exhibited significantly higher FC values than the PD patients with normal olfaction or the PD patients with mild to moderate microsomia. Except for the olfactory performance, no significant correlation was detected between the neuropsychological assessments and the FC values. A linear regression analysis revealed that the increased FC and Geriatric Depression Scale are independently associated with lower the University of Pennsylvania Smell Identification Test scores. The current findings enhanced the understanding of olfactory dysfunction-related pathophysiological mechanisms in early PD and suggested that the left EC-FC in the right dCC may be a potential neuroimaging biomarker for olfactory performance.
PubMed: 35892404
DOI: 10.3390/brainsci12080963 -
Neuroscience Research Sep 2022New neurons are constantly generated in the olfactory bulb and the dentate gyrus of the hippocampus. The number of new cells depends on sensory experiences; an enriched...
New neurons are constantly generated in the olfactory bulb and the dentate gyrus of the hippocampus. The number of new cells depends on sensory experiences; an enriched odor environment increases neurogenesis and neural survival. The aim of this study was to investigate whether enriched olfactory stimuli affect neurogenesis of mitral and granule cells of the olfactory bulb and dentate gyrus, and whether respiratory activity accompanied by olfactory stimuli is associated with new cells in these regions. To this end, respiratory activity during enriched odor stimuli was continuously measured in mice and new cells were stained with 5-bromo-2'-deoxyuridine, which selectively labels proliferating cells. An enriched olfactory environment significantly increased neurogenesis of mitral and granule cells in the olfactory bulb, but not in the dentate gyrus. Additionally, an increase of new granule cells under the enriched odor condition was correlated to sniffing frequency power, which had a significantly different pattern from the no-odor condition. A high respiratory frequency with frequent odor stimuli may be associated with activation of granule cells to form inhibitory neurons and this active state might increase granule cell neurogenesis.
Topics: Animals; Mice; Neurogenesis; Neurons; Odorants; Olfactory Bulb; Smell
PubMed: 35636589
DOI: 10.1016/j.neures.2022.05.007 -
Brain Structure & Function Jan 2022Brain structural features of healthy individuals are associated with olfactory functions. However, due to the pathophysiological differences, congenital and acquired...
Brain structural features of healthy individuals are associated with olfactory functions. However, due to the pathophysiological differences, congenital and acquired anosmia may exhibit different structural characteristics. A systematic review was undertaken to compare brain structural features between patients with congenital and acquired anosmia. A systematic search was conducted using PubMed/MEDLINE and Scopus electronic databases to identify eligible reports on anosmia and structural changes and reported according to PRISMA guidelines. Reports were extracted for information on demographics, psychophysical evaluation, and structural changes. Then, the report was systematically reviewed based on various aetiologies of anosmia in relation to (1) olfactory bulb, (2) olfactory sulcus, (3) grey matter (GM), and white matter (WM) changes. Twenty-eight published studies were identified. All studies reported consistent findings with strong associations between olfactory bulb volume and olfactory function across etiologies. However, the association of olfactory function with olfactory sulcus depth was inconsistent. The present study observed morphological variations in GM and WM volume in congenital and acquired anosmia. In acquired anosmia, reduced olfactory function is associated with reduced volumes and thickness involving the gyrus rectus, medial orbitofrontal cortex, anterior cingulate cortex, and cerebellum. These findings contrast to those observed in congenital anosmia, where a reduced olfactory function is associated with a larger volume and higher thickness in parts of the olfactory network, including the piriform cortex, orbitofrontal cortex, and insula. The present review proposes that the structural characteristics in congenital and acquired anosmia are altered differently. The mechanisms behind these changes are likely to be multifactorial and involve the interaction with the environment.
Topics: Anosmia; Brain; Gray Matter; Humans; Magnetic Resonance Imaging; Olfaction Disorders
PubMed: 34635958
DOI: 10.1007/s00429-021-02397-3 -
Journal of Clinical Medicine May 2023The efficacy of electroconvulsive therapy (ECT) in the treatment of adolescents with treatment-refractory depression is still unsatisfactory, and the individual...
OBJECTS
The efficacy of electroconvulsive therapy (ECT) in the treatment of adolescents with treatment-refractory depression is still unsatisfactory, and the individual differences are large. It is not clear which factors are related to the treatment effect. Resting-state fMRI may be a good tool to predict the clinical efficacy of this treatment, and it is helpful to identify the most suitable population for this treatment.
METHODS
Forty treatment-refractory depression adolescents were treated by ECT and evaluated using HAMD and BSSI scores before and after treatment, and were then divided into a treatment response group and a non-treatment group according to the reduction rate of the HAMD scale. We extracted the ALFF, fALFF, ReHo, and functional connectivity of patients as predicted features after a two-sample -test and LASSO to establish and evaluate a prediction model of ECT in adolescents with treatment-refractory depression.
RESULTS
Twenty-seven patients achieved a clinical response; symptoms of depression and suicidal ideation were significantly improved after treatment with ECT, which was reflected in a significant decrease in the scores of HAMD and BSSI ( < 0.001). The efficacy was predicted by ALFF, fALFF, ReHo, and whole-brain-based functional connectivity. We found that models built on a subset of features of ALFF in the left insula, fALFF in the left superior parietal gyrus, right superior parietal gyrus, and right angular, and functional connectivity between the left superior frontal gyrus, dorsolateral-right paracentral lobule, right middle frontal gyrus, orbital part-left cuneus, right olfactory cortex-left hippocampus, left insula-left thalamus, and left anterior cingulate gyrus-right hippocampus to have the best predictive performance (AUC > 0.8).
CONCLUSIONS
The local brain function in the insula, superior parietal gyrus, and angular gyrus as well as characteristic changes in the functional connectivity of cortical-limbic circuits may serve as potential markers for efficacy judgment of ECT and help to provide optimized individual treatment strategies for adolescents with depression and suicidal ideation in the early stages of treatment.
PubMed: 37240663
DOI: 10.3390/jcm12103556 -
Chemical Senses Jan 2022The brain forms robust associations between odors and emotionally salient memories, making odors especially effective at triggering fearful or traumatic memories. Using...
The brain forms robust associations between odors and emotionally salient memories, making odors especially effective at triggering fearful or traumatic memories. Using Pavlovian olfactory fear conditioning (OFC), a variant of the traditional tone-shock paradigm, this study explored the changes involved in its processing. We assessed the expression of neuronal plasticity markers phosphorylated cyclic adenosine monophosphate response element binding protein (pCREB) and phosphorylated mitogen-activated protein kinase (pMAPK) 24 h and 14 days following OFC, in newborn neurons (EdU+) and in brain regions associated with olfactory memory processing; the olfactory bulb, piriform cortex, amygdale, and hippocampus. Here, we show that all proliferating neurons in the dentate gyrus of the hippocampus and glomerular layer of the olfactory bulb were colocalized with pCREB at 24 h and 14 days post-conditioning, and the number of proliferating neurons at both time points were statistically similar. This suggests the occurrence of long-term potentiation within the neurons of this pathway. Finally, OFC significantly increased the density of pCREB- and pMAPK-positive immunoreactive neurons in the medial and cortical subnuclei of the amygdala and the posterior piriform cortex, suggesting their key involvement in its processing. Together, our investigation identifies changes in neuroplasticity within critical neural circuits responsible for olfactory fear memory.
Topics: Amygdala; Cell Proliferation; Fear; Humans; Infant, Newborn; Piriform Cortex; Smell
PubMed: 35997758
DOI: 10.1093/chemse/bjac021 -
Frontiers in Neurology 2022Traumatic brain injury is one of the major causes of human olfactory dysfunction and leads to brain structure alterations, mainly in the cortical olfactory regions. Our...
OBJECTIVE
Traumatic brain injury is one of the major causes of human olfactory dysfunction and leads to brain structure alterations, mainly in the cortical olfactory regions. Our study aimed to investigate volume changes in the gray matter (GM) and white matter (WM) in patients with post-traumatic anosmia and then to explore the relationship between GM volume and olfactory function.
METHODS
Ethics committee approved prospective studies which included 22 patients with post-traumatic anosmia and 18 age- and gender-matched healthy volunteers. Olfactory function was assessed using the Sniffin' Sticks. High-resolution 3-dimensional T1 MRIs of the participants were acquired on a 3T scanner and the data were collected for voxel-based morphometry (VBM) analysis. Furthermore, the GM and WM volumes of the whole brain regions were compared and correlated with olfactory function.
RESULTS
The analysis revealed significant GM volume reduction in the orbitofrontal cortex (OFC), gyrus rectus (GR), olfactory cortex, insula, parahippocampal, temporal pole, and cerebellum (all < 0.001) in patients. Besides, WM volume loss was also found in the OFC, GR, and insula (all < 0.001) in patients. All WM atrophy areas were connected to areas of GM volume loss spatially. Correlation analysis showed the olfactory scores were significantly positively correlated with the GM volume of the occipital cortex ( < 0.001, and < 0.05), while no significant correlation was found between the Sniffin' Sticks test scores and the WM volume in patients.
CONCLUSION
The reduction of GM and WM volume in olfactory-related regions was responsible for olfactory dysfunction in post-traumatic patients. The occipital cortex may play a compensation mechanism to maintain the residual olfactory function. To our knowledge, we report here for the first time on white matter volume alterations specifically in post-traumatic patients with anosmia.
PubMed: 35860485
DOI: 10.3389/fneur.2022.690760 -
Frontiers in Cellular and Infection... 2022Ocular infection with causes toxoplasmosis in mice. However, following ocular infection with tachyzoites, the cause of the accompanying progressive changes in...
Ocular infection with causes toxoplasmosis in mice. However, following ocular infection with tachyzoites, the cause of the accompanying progressive changes in hippocampal-dependent tasks, and their relationship with the morphology and number of microglia, is less well understood. Here, in 6-month-old, female BALB/c mice, 5 μl of a suspension containing 48.5 × 10 tachyzoites/ml was introduced into the conjunctival sac; control received an equal volume of saline. Before and after instillation, all mice were subject to an olfactory discrimination (OD) test, using predator (cat) feces, and to an open-field (OF) task. After the behavioral tests, the animals were culled at either 22 or 44 days post-instillation (dpi), and the brains and retinas were dissected and processed for immunohistochemistry. The total number of Iba-1-immunolabeled microglia in the molecular layer of the dentate gyrus was estimated, and three-dimensional reconstructions of the cells were evaluated. Immobility was increased in the infected group at 12, 22, and 43 dpi, but the greatest immobility was observed at 22 dpi and was associated with reduced line crossing in the OF and distance traveled. In the OD test, infected animals spent more time in the compartment with feline fecal material at 14 and at 43 dpi. No OD changes were observed in the control group. The number of microglia was increased at 22 dpi but returned to control levels by 44 dpi. These changes were associated with the differentiation of tachyzoites into bradyzoite-enclosed cysts within the brain and retina. Thus, infection of mice with alters exploratory behavior, gives rise to a loss in predator's odor avoidance from 2 weeks after infection, increased microglia number, and altered their morphology in the molecular layer of the dentate gyrus.
Topics: Animals; Cats; Conjunctiva; Female; Mice; Mice, Inbred BALB C; Neuropathology; Toxoplasma; Toxoplasmosis, Animal
PubMed: 35372100
DOI: 10.3389/fcimb.2022.812152 -
Diabetes, Metabolic Syndrome and... 2021The purpose of the study was to find the differences in intrinsic functional connectivity (FC) patterns of the primary visual area (V1) among diabetic retinopathy (DR),...
OBJECTIVE
The purpose of the study was to find the differences in intrinsic functional connectivity (FC) patterns of the primary visual area (V1) among diabetic retinopathy (DR), diabetes mellitus (DM), and healthy controls (HCs) applying resting-state functional magnetic resonance imaging (rs-fMRI).
PATIENTS AND METHODS
Thirty-five subjects with DR (18 males and 17 females), 22 DM (10 males and 12 females) and 38 HCs (16 males and 22 females) matched for sex, age, and education underwent rs-fMRI scanning. Seed-based FC analysis was performed to find the alterations in the intrinsic FC patterns of V1 in DR compared with DM and HCs.
RESULTS
The study found that DR patients had a significant lower FC between the bilateral calcarine (CAL)/left lingual gyrus (LING) (BA 17/18) and the left V1, and between the bilateral CAL/left LING (BA 17/18) and the right V1 compared with the HCs. Meanwhile, patients with DR exhibited higher FC strength between the left V1 and the bilateral Caudate/Olfactory/Orbital superior frontal gyrus (OSFG), and between the bilateral Caudate/Olfactory/OSFG (BA 3/4/6) and the right V1. Compared with DM group, patients with DR showed increased FC strength between the right CAL (BA 17/18) and the right V1. DM group exhibited lower FC strength between the left fusiform and the left V1, and between the bilateral CAL and the right V1 when compared with HCs. Moreover, DM group was observed to have higher FC strength between the left superior frontal gyrus and the left V1.
CONCLUSION
Our findings indicated that DR patients exhibited FC disruptions between V1 and higher visual regions at rest, which may reflect the aberrant information communication in the V1 area of DR individuals. The findings offer important insights into the neuromechanism of vision disorder in DR patients.
PubMed: 34285528
DOI: 10.2147/DMSO.S311009 -
BMC Neuroscience Mar 2021Alzheimer's disease (AD) is characterized by cognitive impairment that eventually develops into dementia. Amyloid-beta (Aβ) accumulation is a widely described hallmark...
BACKGROUND
Alzheimer's disease (AD) is characterized by cognitive impairment that eventually develops into dementia. Amyloid-beta (Aβ) accumulation is a widely described hallmark in AD, and has been reported to cause olfactory dysfunction, a condition considered an early marker of the disease associated with injuries in the olfactory bulb (OB), the hippocampus (HIPP) and other odor-related cortexes. Adiponectin (APN) is an adipokine with neuroprotective effects. Studies have demonstrated that APN administration decreases Aβ neurotoxicity and Tau hyperphosphorylation in the HIPP, reducing cognitive impairment. However, there are no studies regarding the neuroprotective effects of APN in the olfactory dysfunction observed in the Aβ rat model. The aim of the present study is to determine whether the intracerebroventricular (i.c.v) administration of APN prevents the early olfactory dysfunction in an i.c.v Amyloid-beta (Aβ) rat model. Hence, we evaluated olfactory function by using a battery of olfactory tests aimed to assess olfactory memory, discrimination and detection in the Aβ rat model treated with APN. In addition, we determined the number of cells expressing the neuronal nuclei (NeuN), as well as the number of microglial cells by using the ionized calcium-binding adapter molecule 1 (Iba-1) marker in the OB and, CA1, CA3, hilus and dentate gyrus (DG) in the HIPP. Finally, we determined Arginase-1 expression in both nuclei through Western blot.
RESULTS
We observed that the i.c.v injection of Aβ decreased olfactory function, which was prevented by the i.c.v administration of APN. In accordance with the olfactory impairment observed in i.c.v Aβ-treated rats, we observed a decrease in NeuN expressing cells in the glomerular layer of the OB, which was also prevented with the i.c.v APN. Furthermore, we observed an increase of Iba-1 cells in CA1, and DG in the HIPP of the Aβ rats, which was prevented by the APN treatment.
CONCLUSION
The present study describes the olfactory impairment of Aβ treated rats and evidences the protective role that APN plays in the brain, by preventing the olfactory impairment induced by Aβ. These results may lead to APN-based pharmacological therapies aimed to ameliorate AD neurotoxic effects.
Topics: Adiponectin; Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Disease Models, Animal; Injections, Intraventricular; Male; Neuroprotective Agents; Olfaction Disorders; Rats; Rats, Wistar
PubMed: 33653273
DOI: 10.1186/s12868-021-00620-9 -
Frontiers in Aging Neuroscience 2021To explore the relationship between white matter changes and olfactory ability among patients with mild cognitive impairment (MCI) and to develop a tool to predict the...
To explore the relationship between white matter changes and olfactory ability among patients with mild cognitive impairment (MCI) and to develop a tool to predict the development of Alzheimer's disease among patients with MCI. The Montreal Cognitive Assessment (MoCA) was used for cognitive assessments, and the 70% isopropanol test paper was used to evaluate olfactory function. Tract-based spatial statistics, based on the diffusion tensor imaging technology, were used to obtain relevant parameters, and behavioral and imaging results were compared between patients with MCI ( = 36) and healthy older adults ( = 32). The olfactory ability of MCI patients was lower overall, which was positively correlated with the MoCA score. Fractional anisotropy (FA) changes significantly of all parameters. Lower FA regions were mainly located in the corpus callosum, the orbitofrontal gyrus, and the left occipital lobe. The olfactory score was significantly correlated with the FA value of the orbitofrontal gyrus. Fibrous connections in several brain regions, such as the entorhinal cortex, were stronger in patients with MCI. The olfactory ability of MCI patients in our group was positively correlated with the neuropsychological scale results. Impairment in olfactory function was superior to memory deficits for predicting cognitive decline among cognitively intact participants. The fibrous connections in several brain regions, such as the entorhinal cortex, were higher in patients with MCI, which suggested that there may be a compensatory mechanism in the olfactory pathway in MCI patients. The decline in olfactory function may be a significant and useful indicator of neuropathological changes in MCI patients and an effective marker for the development of cognitive decline and dementia.
PubMed: 34887745
DOI: 10.3389/fnagi.2021.765432