Create a PowerPoint presentation regarding the attached article. Discuss the following in the Presentation. Don’t forget to include the Speaker Notes along the slides.
a. Summarize the article; include key points or findings of the article.
b. Discuss how you could use the information in the article for your nursing practice; give specific examples.Zheng et al., Sci. Adv. 2019; 5 : eaau8317 6 February 2019
S C I E N C E A D V A N C E S | R E S E A R C H A R T I C L E
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N E U R O S C I E N C E
The gut microbiome from patients with schizophrenia
modulates the glutamate-glutamine-GABA cycle and
schizophrenia-relevant behaviors in mice
Peng Zheng1,2,3*, Benhua Zeng4*, Meiling Liu5, Jianjun Chen6, Junxi Pan2,3,7, Yu Han1,2,3,
Yiyun Liu1,2,3, Ke Cheng1,2,3, Chanjuan Zhou2,3, Haiyang Wang1,2,3, Xinyu Zhou1,2,3, Siwen Gui1,2,3,
Seth W. Perry8, Ma-Li Wong8, Julio Licinio8†‡, Hong Wei9†‡, Peng Xie1,2,3†‡
Schizophrenia (SCZ) is a devastating mental disorder with poorly defined underlying molecular mechanisms. The
gut microbiome can modulate brain function and behaviors through the microbiota-gut-brain axis. Here, we
found that unmedicated and medicated patients with SCZ had a decreased microbiome -diversity index and
marked disturbances of gut microbial composition versus healthy controls (HCs). Several unique bacterial
taxa (e.g., Veillonellaceae and Lachnospiraceae) were associated with SCZ severity. A specific microbial panel
(Aerococcaceae, Bifidobacteriaceae, Brucellaceae, Pasteurellaceae, and Rikenellaceae) enabled discriminating
patients with SCZ from HCs with 0.769 area under the curve. Compared to HCs, germ-free mice receiving SCZ
microbiome fecal transplants had lower glutamate and higher glutamine and GABA in the hippocampus and
displayed SCZ- relevant behaviors similar to other mouse models of SCZ involving glutamatergic hypofunction.
Together, our findings suggest that the SCZ microbiome itself can alter neurochemistry and neurologic function
in ways that may be relevant to SCZ pathology.
Schizophrenia (SCZ) is a devastating illness affecting approximately
0.5 to 1% of the general population worldwide (1). Previously, re-
searchers have focused on analysis of the human genome to determine
the pathogenesis of SCZ (2). Genome-wide association (GWAS)
analysis of 36,000 patients identified 108 susceptibility loci for SCZ
(3). However, the identified associations likely account for only about
4% of the variance in SCZ. Thus, we should also seek to identify the
role of non-human genetic factors in the onset of SCZ.
The gastrointestinal (GI) tract is a complex ecosystem contain-
ing a large number of resident microorganisms (4). Recent evidence
suggests that the gut microbiota could modulate brain function and
behaviors via the “microbiota-gut-brain” (MGB) axis (5, 6). For ex-
ample, gut microbiota have been reported to be associated with al-
terations in anxiety (7), memory (8), cognition (9), and locomotor
activity (10). Our groups recently showed that modulation of gut
microbiota using the germ-free (GF) method or antibiotics could
result in depressive-like behaviors (11, 12). These findings highlight
the novel possibility that disturbances of gut microbiota or the MGB
axis may contribute to the onset of psychiatric disorders.
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