Local area community cumulative incidence (per 1,000 population) Health care personnel with positive test results for SARS-CoV-2 antibodies (%) Abbreviation: COVID-19 = coronavirus disease 2019. * Calculated as the total number of reported community COVID-19 cases within a hospital-area county or counties between the beginning of the pandemic and 7 days after the first day of health care personnel enrollment at the hospital divided by population of the county or counties x 1,000.

Aromatic L-amino acid decarboxylase (AAAD) activity is enhanced in the striatum of control and MPTP-treated mice after administration of a single dose of the dopamine receptor antagonists haloperidol, sulpiride, and SCH 23390. MPTP-treated mice appear more sensitive to the antagonists, i.e., respond earlier and to lower doses of antagonists than control mice. The rise of AAAD activity induced by the antagonists is prevented by pretreatment with cycloheximide. The apparent Km values for L-3,4-dihydroxyphenylalanine (L-DOPA) and pyridoxal 5-phosphate appear unchanged after treatment with the antagonists. Increased AAAD activity was observed also after subchronic administration of dopamine receptor antagonists or treatment with reserpine. A single dose of a selective dopamine receptor agonists had no effect on AAAD activity. In contrast, administration of L-DOPA, quinpirole, or SKF 23390 for 7 days lowers AAAD activity in the striatum. We conclude that AAAD is modulated in striatum via dopaminergic receptors.

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A single dose of nicotine increased methionine‐enkephalin (Met‐Enk) immunoreactivity in the striatum of mice in a time‐dependent manner. Met‐Enk content reached a maximum by ∼1 h after nicotine and returned to control values by 6 h. The response to nicotine was blocked by pretreating animals with the nicotinic receptor antagonist mecamylamine. In contrast, pretreating mice with the muscarinic receptor antagonist atropine or the dopamine receptor antagonist haloperidol did not block the response. A single dose of nicotine also increased mRNA for the precursor peptide preproenkephalin (PPE). The increase of PPE mRNA preceded that of Met‐Enk and reached a maximum by ∼30 min after nicotine. PPE mRNA levels returned to near normal by ∼3 h and increased again by 6 h after nicotine. Daily administration of nicotine for 14 days increased Met‐Enk content and PPE mRNA in the striatum of mice as well. Taken together, our results suggest that nicotinic receptors modulate Met‐Enk content and PPE mRNA in the mouse striatum.

Selective neuronal vulnerability to protein aggregation is found in many neurodegenerative diseases including Alzheimer's disease (AD). Understanding the molecular origins of this selective vulnerability is therefore of fundamental importance. Tau protein aggregates have been found in manuscriptClick here to access/download;manuscript;Manuscript_Final submission.docx Click here to view linked References Wolframin (WFS1)-expressing excitatory neurons in the entorhinal cortex, one of the earliest affected regions in AD. The role of WFS1 in Tauopathies and its levels in tau pathology-associated neurodegeneration, however, is largely unknown. Here we report WFS1 deficiency is associated with increased tau pathology and neurodegeneration, whereas overexpression of WFS1 reduces those changes. We also find that WFS1 interacts with tau protein and controls the susceptibility to tau pathology. Furthermore, chronic ER stress-and autophagy-lysosome pathway (ALP)associated genes are enriched in WFS1-high excitatory neurons in human AD at early Braak stages.The protein levels of ER stress-and autophagy-lysosome pathway (ALP)-associated proteins are changed in tau transgenic mice with WFS1 deficiency, while overexpression of WFS1 reverses those changes. This work demonstrates a possible role for WFS1 in the regulation of tau pathology and neurodegeneration via chronic ER stress and the downstream ALP. Our findings provide insights into mechanisms that underpin selective neuronal vulnerability, and for developing new therapeutics to protect vulnerable neurons in AD.