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The human brain is an amazing organ, capable of surprising feats of memory, susceptible to damage, and yet remarkably adaptable to change. It does so much but what is the actual size of the brain? While the human brain has a structure similar to that of other mammals, what makes it so very different is its size in relation to body size. Compared to the size of our bodies, human beings have much larger brains than many other mammals. Obviously, not all people have the same size brain.

Neurons are the structures that serve as building blocks of the brain and nervous system. They transmit and carry information, allowing different parts of the brain to communicate with one another as well as allowing the brain to communicate with various parts of the body. Researchers estimate that there are around billion neurons in the human brain.

Genetic and Environmental Factors Influence Intelligence. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Article Sources. Verywell Mind uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles.

Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy. Hoag, H.

Sex on the Brain. New Scientist. July 19, May 3, Related Articles. As expected, mock-infused mice learned the novel object recognition NOR memory task, as demonstrated by longer exploration of the novel object over the familiar one Fig.

ZIKV-infected mice further showed memory impairment in a hippocampus-dependent task, the passive avoidance step-down paradigm Fig.

Interestingly, performances of infected mice in both NOR Fig. ZIKV causes synapse damage and memory impairment in mice. Adult mice received an i. Representative images of the CA3 hippocampal region of mock-infused g, l or ZIKV-infected mice h, m at 6 gh and 60 l, m dpi, immunolabeled for synaptophysin SYP, green and Homer1 red.

Symbols represent individual mice a - p or individual slices s-t. Source data from panels a-fi-kn-t are provided as Source Data File. To further investigate if impairment triggered by ZIKV could be a non-specific response triggered by replication of any arbovirus, mice were infected i. Viral infections may cause non-specific behavioral symptoms known as sickness behavior Mock-infused and ZIKV-infected mice showed similar exploratory behavior when sequentially evaluated in an open-field arena from 1 to 60 dpi Supplementary Fig.

At longer evaluation times in the same task during acute infection, both experimental groups showed the expected habituation behavior Supplementary Fig. Further, both groups explored similarly the center of the open-field arena and the open arms of the elevated plus maze Supplementary Fig.

Additional control measurements showed that neither groups of mice had innate preferences for the objects used in the NOR memory test Supplementary Fig.

Synapse damage is a common denominator in a number of memory-affecting conditions We thus investigated whether infection by ZIKV-induced synapse damage.

Decreased colocalization between synaptophysin SYP, a pre-synaptic marker and Homer-1 a post-synaptic marker immunoreactive puncta, a measure of synaptic density, was observed in hippocampal CA3 region Fig. Because the CA3 hippocampal region was found to be particularly vulnerable to synapse damage Fig. To determine whether synapse damage and inhibition of synaptic plasticity induced by ZIKV were accompanied by neurodegeneration, FluoroJade B FJ staining of brain sections was performed at 6 and 10 dpi.

Inflammation is an important feature of brain viral infections, and has been associated with memory impairment in pathological conditions 3132 Expression of these cytokines was unaffected in the brains of mice infused with iZIKV gray barsindicating that the proinflammatory response required active viral replication. ZIKV triggers brain inflammation and microgliosis in adult mice. Symbols correspond to individual mice. Source data from panels a - eo, q, r, tu are provided as Source Data File.

We next investigated whether gliosis was induced by infection. In contrast, intense Iba-1 immunoreactivity was verified in the brains of ZIKV-infected mice at 6 dpi, notably in the hippocampus Fig. Perivascular cuffings and microglial nodules Fig. Iba-1 immunostaining in hippocampi of ZIKV-infected mice was reduced by 30 dpi and reached control levels at 60 dpi Fig.

Prominent microgliosis was also found in parietal and frontal cortices Supplementary Fig. We thus asked whether striatal viral load and neuroinflammation were associated with impaired performance in the rotarod test, a classical paradigm for assessment of motor function.

ZIKV-infected mice 5 dpi exhibited lower latencies to fall from the rotating rod than mock-infected mice Supplementary Fig. These findings indicate that ZIKV-induced motor dysfunction is reversible and paralleled by microgliosis, similarly to memory impairment. In agreement with lower viral levels in sensory cortex compared to other cortical areas Fig. Further characterization of the cellular response to infection was performed by flow cytometry in brain cell suspensions from mock-and ZIKV-infected mice at 6 dpi.

Pruning of synaptic terminals by microglia is an important mechanism underlying synapse loss in neurodegenerative disorders and in viral infections 31 In line with this, and given the phagocytic appearance of microglia in ZIKV-infected mice, we hypothesized that microglial activation could play a central role in ZIKV-induced synapse damage and memory impairment. Three-dimensional image reconstructions of Ibapositive cells in the hippocampi of ZIKV-infected mice showed synaptophysin-positive terminals inside Ibapositive cells Fig.

Microglia mediates ZIKV-induced memory impairment in mice. White arrows point to SYP-positive elements engulfed within microglia.

Symbols represent individual mice a - In or individual slices l - m.

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Source data from panels cg - n are provided as Source Data File. Next, we evaluated whether blockage of microglial activation could prevent ZIKV-induced memory impairment. For this, we used minocycline, a tetracycline antibiotic that blocks microglial activation Minocycline had no effect on the number of hippocampal Iba-1 positive cells Fig.

Control measurements showed that minocycline had no effect on motivation or anxiety-like behaviors in mice Supplementary Fig. Importantly, infliximab restored memory Fig. Treatment with infliximab had no effect on total object exploration times, anxiety behavior Supplementary Fig. Adult Swiss mice received an i. Symbols correspond to individual mice a - l or individual slices o - p.

The brain is one of the largest and most complex organs in the human body. It is made up of more than billion nerves that communicate in trillions of connections called synapses.

Source data panels d - ei - p are provided as Source Data File. Complement system proteins C1q and C3 have been implicated in synaptic tagging driving microglial recognition and pruning of synapses in the brains of mice infected by West Nile virus WNV Both C1q Fig.

Blockage of microglial activation by minocycline attenuated upregulation of both C3 and C1q Fig. Role of complement system in ZIKV-induced memory impairment. Source data from panel a - f and k - n are provided as Source Data File.

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Soluble C1q and C3 proteins in the brain diffuse and target dysfunctional synapses, signaling for microglial pruning 31 This prompted us to investigate whether blockage of soluble C1q and C3 by i. Control experiments showed that neutralizing each of these proteins in the brain had no effect on locomotion or anxiety behavior Supplementary Fig. Notably, neutralization of either C1q or C3 rescued both hippocampal synapse density Fig.

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ZIKV infection during pregnancy causes serious neurological conditions in newborns, including microcephaly 46. Though initially considered a self-limited febrile state in adults, ZIKV infection was recently linked to the development of neurological complications 891011121314151617181920212223including acute myelitis 1321encephalitis, 810111621 and meningoencephalitis 18 Indeed, ZIKV infection has been associated with increased incidence of a broad spectrum of neurological disorders in adult patients 8.

Moreover, ZIKV has been found in the brains and CSF of adult patients 810111822and recent studies demonstrated that ZIKV persists in CSF and lymph nodes of infected monkeys for several weeks after clearance from peripheral blood, urine, and mucosal secretions Nonetheless, while several lines of evidence indicate that human neural precursor cells are affected by ZIKV 3whether mature neural cells and adult human brain tissue are susceptible to infection by ZIKV remained to be determined.

Addressing this gap, we report that ZIKV replicates in ex vivo slices from adult human cortical tissue. We detected infectious viral particles released to the medium, indicating successful assembly of particles capable of spreading infection. Using immunocompetent mice infused via i. A recent study showed viral replication in the brain in a similar time frame following systemic administration of an Asian ZIKV strain to immunocompromised mice Intriguingly, in that study viral replication was mainly detected at sites of adult neurogenesis.

In contrast, we show replication of the Brazilian ZIKV strain in slices from human adult temporal lobe, a region not considered a classical neurogenic niche. We further show that, in adult mice, the highest viral loads were detected in the hippocampus and frontal cortex, brain regions closely related to cognition, memory and executive function, and in the striatum, a structure involved in motor control.

These findings strengthen the usefulness of our model to unravel the consequences of ZIKV infection in the mature brain. In contrast with the brain regional selectivity for viral replication verified following i. Similar results were found following systemic infection by ZIKV in wild-type mice at post-natal day 3, a stage when interferon-mediated inflammatory response is inefficient.

It appears likely, therefore, that lack of the ability to mount an effective interferon-based response leads to generalized replication of ZIKV across the brain, abolishing the preferential targeting of regions associated with cognitive and motor control verified in immunocompetent adult mice.

This suggests that the brain region-specificity of the host immune response may be an important determinant for the efficiency of viral replication in different brain structures. These findings demonstrate that ZIKV targets memory-related brain regions regardless of whether the route of infection is central or peripheral. They further underline the translational potential of the adult ZIKV infection model used here, since the virus has been detected in CSF of adult patients with neurological complications 10111218 An early study by Bell and colleagues concluded that both neurons and astrocytes were infected by the African strain of ZIKV adapted to mice, leading to hippocampal degeneration and necrosis 7 days post-infection We found no NS2B immunostaining in doublecortin-positive cells at the peak of replication.

However, we found a reduced number of doublecortin-positive cells in the hippocampal dentate gyrus of ZIKV-infected mice. Our results indicate that neurons are the main cell type infected by ZIKV in the adult mouse and human brain. Current findings are in contrast with those reported in the developing brain 3when ZIKV infects both neurons and glia, suggesting that ZIKV may target distinct cell populations at different stages of brain development.

Although our results demonstrate that ZIKV infects neurons, how these cells react to viral infection remains to be elucidated. Previous studies showed that ZIKV-infected neurons activate intracellular innate immune pathways, leading to the release of proinflammatory cytokines 39 Although the mechanisms linking neuronal infection and cytokine production are still a matter of debate, previous studies along with our current results suggest that neurons are both a target of ZIKV infection and a potential source of inflammation.

Viral infections have been associated with neurological damage in humans and mice. Learning and memory are frequently affected, with symptoms often persisting for long periods after the acute phase of the disease 31 We found that brain infection by ZIKV caused memory impairment in adult mice, and that this was accompanied by reduced synaptic density in hippocampal CA3 and DG.

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Our results further indicate that memory impairment induced by ZIKV was not caused by sickness behavior. Results also showed that not all arboviruses cause memory impairment, as mice infected by MAYV had no memory dysfunction. Recent studies have demonstrated memory impairment and synapse pathology in mice following infection by other neuroinvasive viruses, such as HIV 42WNV 31Herpes Simplex virus-1 43and Borna disease virus We further demonstrate that phosphorylated CREB, an important transcription factor involved in memory mechanisms 30was markedly decreased in the hippocampus and cortex of ZIKV-infected mice.

Reactive gliosis has been described in developing brains of mice 32 and in humans exposed to ZIKV in uterus or during adulthood 318 We demonstrate that ZIKV infection triggered marked neuroinflammation and brain microgliosis in adult mice. Microglia play a central role in the pruning of synapses tagged by complement system proteins in a mouse model of WNV infection Significantly, we found that treatments with infliximab or minocycline prevented memory and synapse dysfunction in ZIKV-infected mice.

We note that complement in the CNS in ZIKV-infected mice may originate from both disruption of BBB integrity and infiltration of peripheral immune cells and from activation of resident microglia. These possibilities are supported by our finding that both central and peripheral treatments with infliximab resulted in decreased brain expression of C3.

However, the lack of effect of infliximab on brain C1q expression in ZIKV-infected mice may be related to the capacity of neurons to express C1q 45 Importantly, we show that i. In conclusion, we have established that ZIKV infects and replicates in adult human brain tissue.

Sep 20,   Here we describe the generation and analysis of a transcriptional atlas of the adult human brain, comprising extensive histological analysis and comprehensive microarray profiling of ? neuroanatomically precise subdivisions in two individuals. Transcriptional regulation varies enormously by anatomical location, with different regions and Cited by: Sep 20,   The goal of the Allen Human Brain Atlas is to create a comprehensive map of transcript usage across the entire adult brain, with the emphasis on anatomically complete coverage at a fine nuclear resolution in a small number of high-quality, clinically unremarkable brains profiled with DNA microarrays for quantitative gene-level transcriptome Cited by: Mar 25,   The Adult Brain Does Grow New Neurons After All, Study Says. Study points toward lifelong neuron formation in the human brain's hippocampus, with implications for memory and disease.

Further, our findings identify a possible mechanism underlying neurological complications in adults infected with ZIKV 8910111213141516171819202122 This culminates in synapse dysfunction and memory impairment, in the absence of overt neurodegeneration. This is consistent with the observation that memory impairment was reversible upon resolution of the infection and inflammation, suggesting that cognitive deficits are caused by aberrant signaling mechanisms triggered by infection rather than by neuronal death.

Although the initial wave of the recent ZIKV epidemics in the Americas is now past, the fact that mosquito populations are not under control suggests that the number of infected individuals will likely remain elevated in coming years, and may eventually spread to additional geographical areas.

From a public health perspective, it would be important to assess memory and cognition in infected adults as a potential significant comorbidity of ZIKV infection. Future studies aimed to examine the long-term neurodegenerative impact of ZIKV infection are warranted, not only in developing brains but also in the adult CNS.

Identifying ways to prevent signaling abnormalities leading to brain dysfunction could pave the way to intervention strategies to delay or prevent the development of major neurological conditions in ZIKV-infected individuals. Ernesto T. Marques Jr. Samples were prepared as described elsewhere For determination of viral titers, plaque assays were performed in Vero cells treated with serial dilutions of stocks or samples.

Successful inactivation was confirmed by plaque assay. Viral titer of stocks and samples was determined by plaque assay using Vero cells. Adult human cortical slices were prepared and characterized as described 48with minor modifications.

Human brain

Samples of temporal lobe cortical tissue were obtained from patients with drug-resistant epilepsy subjected to temporal lobectomy. Informed consent was obtained from all participants. Samples used in the current study comprised temporal lobe cortical fragments plus associated subcortical tissue. Medium was harvested at specified time points for determination of viral titers by plaque assay. A mice were weeks-old at the beginning of experiments.

For infusion into the lateral ventricle i. As previously described, a 2. In some experiments, mice received an i. After surgery, the skull was sealed with dental cement, and animals were euthanized 6 days post-infection dpi.

In one experiment, neonatal post-natal day 3 Swiss-mice were submitted to subcutaneous s. Pups were then killed by decapitation at 12 dpi, the peak of viral replication at this age Brains were collected at different time points following infection, homogenized to a concentration of 0. For i. For blockage of brain complement proteins, mice received i. Tissues were homogenized to a concentration of 0. Actin was used as an endogenous control.

Antigens were reactivated by treatment with 0. Identical conditions and reaction times were used for slides from different animals run in parallel to allow comparison between immunoreactivity optical densities. Reactions were stopped by immersion of slides in distilled water. Counter-staining was performed with Harris hematoxylin.

Total pixel intensity was determined for each image and data are expressed as integrated optical density OD. Alternatively, the number of Ibapositive cells per mm 2 was counted. For morphological characterization of Ibapositive cells, we analyzed cell bodies in two dimensions and measured Feret diameters as previously described Maximum and minimum Feret are defined as the longest and shotest diameters of a cell body, respectively.

In a spherical cell body, max-min Feret differences tend to zero. Three independent images of each brain structure were used for analyses. Each image acquired was a z-stack of 0. We used the Puncta Analyzer plugin for ImageJ 1. Averaged puncta values for mock-infused mice controls were used to calculate percentage of puncta results for all groups To determine synapse engulfment by microglia, three confocal Z-stack images from the CA3 hippocampal region from ZIKV-infected or mock-injected mice were acquired using a Nikon CII confocal microscope.

Each image comprised 0. Background from the red channel was subtracted using a 50 pixel radius rolling ball and then subjected to a 2 pixel radius 3D median filter in every dimension. Background and noise from the green channel were subtracted using a 2 pixel rolling ball radius followed by the Despeckle function. The two channels were then merged for puncta analyses using Puncta Analyzer v2.

Our analysis also focused on sex differences in variance. Here, for the first time in an adult sample, we directly tested sex differences in the variance of several brain measures, finding greater male variance across almost the entire brain for volume, surface area, and white matter fractional anisotropy, but only patchy and inconsistent variance differences for cortical thickness and white matter orientation dispersion. Our correlation of the vector of mean differences with that of variance ratios showed that there was some degree of correspondence between them for volume, but the relation was far smaller for surface area and was near-zero for cortical thickness.

In all cases, this analysis indicated that mean and variance differences appear to be largely independent cts of sex differences in the brain; we should not expect to see that areas showing the largest difference in mean also show the largest difference in variance, at least to a great extent. Such explanations are speculative at present; as studies like UK Biobank release even larger amounts of data on individuals who have both neurostructural and genotype data, researchers will be able to perform well-powered tests of these hypotheses.

In discussing any potential genetic effects on sex differences, analyses should take into account the fact that such effects are likely active at multiple points across the lifespan, representing a continuing, complex set of influences that may interact with environment and experience. Using the limited data on cognitive abilities available in our sample, we tested whether the data were consistent with any consequences of brain structural differences in terms of ability differences.

There were only weak correlations between brain variables and the cognitive tests consistent with previous evidence of these links: Karama et al. Perhaps unexpectedly, given evidence and theory linking white matter microstructure to cognitive processing speed Penke et al.

Cortical thickness had trivial mediating effects compared to volume and surface area: no more than 7. With our multiple-mediator models, we built a map of which brain regions were most relevant in this mediation of the sex-cognitive relation Fig.

Overall, the data were consistent with higher volume and cortical surface area-but not cortical thickness or microstructural characteristics-chiefly in the superior temporal region, but also spread across multiple other regions to a lesser extent, being of particular relevance to sex differences in reasoning but not reaction time. An additional hypothesis-one that is not incompatible with the hypothesis that some of the sex differences seen here are a proximate cause of behavioral differences-is that brain structural differences might sometimes be the result of compensatory mechanisms for differences in sex-specific hormones, and might thus act to reduce behavioral sex differences that would otherwise have been present De Vries ; McCarthy and Arnold This perspective may in part explain an apparent paradox in human sex difference research: that the raw effect sizes found for brain measures such as volume and surface area are so large, whereas most behavioral sex differences are so small Hyde Our descriptive results do not directly speak to any causal mechanisms, but it should be borne in mind that they are compatible with these multiple interpretations.

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Sex differences in intrinsic functional connectome organization also revealed results that corroborate and extend prior work. Whether such an effect can help explain higher average female ability in domains like social cognition Gur et al. Finally, recent work has shown that intrinsic functional connectome organization can be parsimoniously described as a small number of connectivity gradients Margulies et al. The most prominent connectivity gradient has at one pole the DMN and at the other unimodal sensory and motor cortices.

The observed pattern of sex differences in functional connectome organization observed here appears to recapitulate the two main poles of that principal connectivity gradient Margulies et al. One potential way of describing the biological significance of these functional sex differences is that mechanisms involved in shaping sex differences biological, cultural, or developmental may influence this principal connectivity gradient; the result, which should be explored in future investigations of brain sex differences, may be the multiple network differences found in the present study.

The UK Biobank sample was selective. It covered only one part of the life course from approximately 45 to 75 years of ageand thus our findings may not apply to younger adults.

May 16,   Here, we report a study that characterizes multimodal sex differences in the adult human brain in the largest sample to date. It is of particular importance to gain a more detailed picture of how the brains of males and females differ, because several psychiatric disorders and conditions differ in their prevalence between the by: Sep 05,   ZIKV replicates in adult human brain tissue. Since ZIKV has been detected in the brains and CSF of adult patients 8,10,12,18,22, we first investigated Cited by: 4. Sep 28,   The human brain is the command center for the human nervous system. It receives signals from the body's sensory organs and outputs information to the muscles.

With ageing may come larger variation in some brain parameters Cox et al. Many of the female participants might have been undergoing, or have undergone, menopause; this or associated Hormone Replacement Therapy might exert modest effects on the structure of some regions of the brain Zhang et al.

In addition, UK Biobank had a very low response rate to invitations to participate 5. We would thus expect the individuals studied here would not be fully representative of males and females from the general UK population. This was the case for education: individuals with college or university degrees were over-represented see Metho though the male:female education ratio itself appeared representative.

These selection effects may in part explain the differences between our results and those of previous studies and meta-analyses, as discussed above. Although we adjusted for the effects of age, it should also be noted-as for any study with a relatively wide age range-that there was substantial variation in the birth date of the participants, undoubtedly leading to different unmeasured social experiences during their development. On the topic of age adjustment, it should also be noted that we adjusted for linear effects of age, whereas some variables may have nonlinear trends although, given a preliminary analysis as described in the Supplemental Materialswe would not expect this to affect the sex differences in these variables to a substantial extent.

We should also note that, as described in the Supplementary Materialsthere was a significant, yet small, age difference between the sexes men were older by 1. A final issue of representativeness concerns clinical outcomes. Although we noted above that there is much interest in sex-differential patterns of psychiatric disorder diagnoses, the unrepresentativeness of UK Biobank extends to generally low rates of such disorders in general in the sample.

For this reason, we did not attempt to link the MRI sex differences observed here to clinical diagnoses, though studies of normal-range variation in traits linked to psychiatric disease such as neuroticism, a known risk factor for Major Depressive Disorder; Kotov et al.

Caution should be taken in interpreting the results of the analyses involving the cognitive tests the mediation analyses in addition to the correlations. Whereas previous, representative studies e. This may be due to problems of sample representativeness Dykiert et al.

The cognitive measures were relatively psychometrically poor compared to a full IQ assessment: the verbal-numerical reasoning test had only 13 items, and the reaction time test had only 4 trials that counted towards the final score see Lyall et al. Although the tests-particularly verbal-numerical reasoning-have some external validity Hagenaars et al.

Fuller cognitive testing, currently underway in UK Biobank, will allow a more comprehensive exploration. Studies that use tests where males or females are known to show higher average scores such as 3D mental rotation tests, which generally show higher scores in males; Maeda and Yoonwould potentially allow for more informative results. In addition, cross-sectional mediation models of observational data, such as those used here, are inherently limited: they cannot address causal relations between variables.

The models were simple, including only 3 main variables sex, the brain measure, and cognitive ability; Fig. Note also that there exists a great deal of debate over testing the quantifying the indirect effect in mediation models e.

More complex models, using longitudinal data and latent variables derived from multiple cognitive tests, should be specified in future research. Finally, although this study used a wide variety of neuroimaging measures, it should be noted that these were but a small selection of the possible modalities that we could have investigated, and that studies should address in future. Other diffusion and NODDI measures of white matter microstructure such as radial and axial diffusivity and intracellular volume fraction Cox et al.

The present study is the largest single-sample study of neuroanatomical sex differences to date. We report evidence on the pattern of sex differences in brain volume, surface area, cortical thickness, white matter microstructure, and functional connectivity between adult males and females in the range between middle- and older-age.

As has previously been argued Fineproviding a clear characterization of neurobiological sex differences is a step towards understanding patterns of differential prevalence in neurodevelopmental disorders such as autism spectrum disorder Baron-Cohen et al.

We hope that the results provided here, given their large-scale, multimodal nature, will constitute an authoritative point of reference for future studies on a wide range of questions on brain sex differences. Insights into how and where the brain differs as a function of sex-with considerably more precision than in previous investigations-will enable more targeted examinations into potential drivers of these differences across psychiatric, psychological, and other domains.

In particular, integrating macrostructural, microstructural, and functional data is an important long-term goal Gur and Gur Data on many thousands of further MRI scans to a maximum sample ofwith MRI data will be available from UK Biobank in the coming years, in addition to more complex cognitive testing batteries and genotypic data.

Future studies will be able to explore in much greater depth the links between sex differences in the brain, their possible causes, and their potential medical and behavioral consequences. Supplementary material is available at Cerebral Cortex online. Authors S. Author S. Author I. Author X. Author L. Author H. Authors A. Author A. We are grateful to the UK Biobank members for their participation in the study, and to the UK Biobank team, who collected, processed, and made available the data for analysis.

This work was carried out under UK Biobank application number 10 None of the funders or other acknowledged individuals are responsible for our analysis or interpretation of our results. Conflict of interest : None declared.

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Basic Parts of the Brain - Part 1 - 3D Anatomy Tutorial

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