scholarly journals The Pandemic Brain: neuroinflammation in healthy, non-infected individuals during the COVID-19 pandemic

2021 ◽  
Author(s):  
Ludovica Brusaferri ◽  
Zeynab Alshelh ◽  
Daniel Martins ◽  
Minhae Kim ◽  
Akila Weerasekera ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Human Brain ◽  
Constitutive Expression ◽  
Symptom Burden ◽  
Brain Regions ◽  
Translocator Protein ◽  
Brain Atlas ◽  
Resonance Spectroscopy ◽  
Positron Emission ◽  
The Impact

The impact of COVID-19 on human health extends beyond the morbidity and death toll directly caused by the SARS-CoV-2 virus. In fact, accumulating evidence indicates a global increase in the incidence of fatigue, brain fog and depression, including among non-infected, since the pandemic onset. Motivated by previous evidence linking those symptoms to neuroimmune activation in other pathological contexts, we hypothesized that subjects examined after the enforcement of lockdown/stay-at-home measures would demonstrate increased neuroinflammation. We performed simultaneous brain Positron Emission Tomography / Magnetic Resonance Imaging in healthy volunteers either before (n=57) or after (n=15) the 2020 Massachusetts lockdown, using [11C]PBR28, a radioligand for the glial marker 18 kDa translocator protein (TSPO). First, we compared [11C]PBR28 signal across pre- and post-lockdown cohorts. Then, we evaluated the link between neuroinflammatory signals and scores on a questionnaire assessing mental and physical impacts of the pandemic. Further, we investigated multivariate associations between the spatial pattern of [11C]PBR28 post-lockdown changes and constitutive brain gene expression in post-mortem brains (Allen Human Brain Atlas). Finally, in a subset (n=13 pre-lockdown; n=11 post-lockdown), we also used magnetic resonance spectroscopy to quantify brain (thalamic) levels of myoinositol (mIns), another neuroinflammatory marker. Both [11C]PBR28 and mIns signals were overall stable pre-lockdown, but markedly elevated after lockdown, including within brain regions previously implicated in stress, depression and 'sickness behaviors'. Moreover, amongst the post-lockdown cohort, subjects endorsing higher symptom burden showed higher [11C]PBR28 PET signal compared to those reporting little/no symptoms. Finally, the post-lockdown [11C]PBR28 signal changes were spatially aligned with the constitutive expression of several genes highly expressed in glial/immune cells and/or involved in neuroimmune signaling. Our results suggest that pandemic-related stressors may have induced sterile neuroinflammation in healthy individuals that were not infected with SARS-CoV-2. This work highlights the possible impact of the COVID-19 pandemic-related lifestyle disruptions on human brain health.

The Parieto-Frontal Integration Theory (P-FIT) of intelligence: Converging neuroimaging evidence

2007 ◽  
Vol 30 (2) ◽  
pp. 135-154 ◽  
Author(s):  
Rex E. Jung ◽  
Richard J. Haier
Keyword(s):  
Individual Differences ◽  
Magnetic Resonance ◽  
Diffusion Tensor ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Temporal Lobectomy ◽  
Integration Theory ◽  
Resonance Spectroscopy ◽  
Positron Emission ◽  
Imaging Research

Abstract“Is there a biology of intelligence which is characteristic of the normal human nervous system?” Here we review 37 modern neuroimaging studies in an attempt to address this question posed by Halstead (1947) as he and other icons of the last century endeavored to understand how brain and behavior are linked through the expression of intelligence and reason. Reviewing studies from functional (i.e., functional magnetic resonance imaging, positron emission tomography) and structural (i.e., magnetic resonance spectroscopy, diffusion tensor imaging, voxel-based morphometry) neuroimaging paradigms, we report a striking consensus suggesting that variations in a distributed network predict individual differences found on intelligence and reasoning tasks. We describe this network as theParieto-Frontal Integration Theory(P-FIT). The P-FIT model includes, by Brodmann areas (BAs): the dorsolateral prefrontal cortex (BAs 6, 9, 10, 45, 46, 47), the inferior (BAs 39, 40) and superior (BA 7) parietal lobule, the anterior cingulate (BA 32), and regions within the temporal (BAs 21, 37) and occipital (BAs 18, 19) lobes. White matter regions (i.e., arcuate fasciculus) are also implicated. The P-FIT is examined in light of findings from human lesion studies, including missile wounds, frontal lobotomy/leukotomy, temporal lobectomy, and lesions resulting in damage to the language network (e.g., aphasia), as well as findings from imaging research identifying brain regions under significant genetic control. Overall, we conclude that modern neuroimaging techniques are beginning to articulate a biology of intelligence. We propose that the P-FIT provides a parsimonious account for many of the empirical observations, to date, which relate individual differences in intelligence test scores to variations in brain structure and function. Moreover, the model provides a framework for testing new hypotheses in future experimental designs.

scholarly journals Cellular sources of TSPO expression in healthy and diseased brain

2021 ◽  
Author(s):  
Erik Nutma ◽  
Kelly Ceyzériat ◽  
Sandra Amor ◽  
Stergios Tsartsalis ◽  
Philippe Millet ◽  
...  
Keyword(s):  
Cell Activity ◽  
Brain Regions ◽  
Cellular Level ◽  
Translocator Protein ◽  
Disease Stage ◽  
Animal Models Of Disease ◽  
Positron Emission ◽  
Neuropsychiatric Diseases ◽  
Tspo Expression

AbstractThe 18 kDa translocator protein (TSPO) is a highly conserved protein located in the outer mitochondrial membrane. TSPO binding, as measured with positron emission tomography (PET), is considered an in vivo marker of neuroinflammation. Indeed, TSPO expression is altered in neurodegenerative, neuroinflammatory, and neuropsychiatric diseases. In PET studies, the TSPO signal is often viewed as a marker of microglial cell activity. However, there is little evidence in support of a microglia-specific TSPO expression. This review describes the cellular sources and functions of TSPO in animal models of disease and human studies, in health, and in central nervous system diseases. A discussion of methods of analysis and of quantification of TSPO is also presented. Overall, it appears that the alterations of TSPO binding, their cellular underpinnings, and the functional significance of such alterations depend on many factors, notably the pathology or the animal model under study, the disease stage, and the involved brain regions. Thus, further studies are needed to fully determine how changes in TSPO binding occur at the cellular level with the ultimate goal of revealing potential therapeutic pathways.

scholarly journals Quantitative lithium magnetic resonance spectroscopy in the normal human brain on a 3 T clinical scanner

2011 ◽  
Vol 66 (4) ◽  
pp. 945-949 ◽  
Author(s):  
Fiona E. Smith ◽  
David A. Cousins ◽  
Peter E. Thelwall ◽  
I. Nicol Ferrier ◽  
Andrew M. Blamire
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Human Brain ◽  
Resonance Spectroscopy ◽  
Normal Human Brain ◽  
Normal Human ◽  
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