Neurodegenerative diseases (NDDs) comprise a broad range of progressive neurological disorders with multifactorial etiology contributing to disease pathophysiology. GEMs and omics integration, that would allow the design of sustainable personalized anti-inflammatory diets in NDDs prevention, through the modulation of gut microbiota was described. was observed in PD. When comparing the mucosa between PD individuals and controls, PD patients demonstrated significantly increased abundance of putative, pro-inflammatory Proteobacteria of the genus spp., spp., spp., spp. and of the family Prevotellaceae in individuals diagnosed with PD, and increases of (Gerhardt and Mohajeri, 2018). Another study, implementing pyrosequencing of the 16S rRNA gene, analyzed the gut microbiota from stool samples of 72 PD patients and 72 healthy controls. Prevotellaceae was reduced by 77.6% in individuals diagnosed with PD. Furthermore, Enterobacteriaceae abundance was positively correlated with motor impairment, evaluated by severity of postural instability and gait difficulty, suggesting that perturbations of the PD microbiome are related to disease-motor phenotype (Scheperjans et al., 2015). Recently, a metagenomic shotgun analysis was performed in order to infer functional implications of alterations in the microbial and viral gut metagenome of 31 early stage L-DOPA-naive PD individuals, Benzocaine having 28 age-matched controls for comparison. This approach found significantly improved abundances of (autopsy (Nussbaum and Ellis, 2003). To clinical manifestations Accordingly, the hippocampus, needed for memory space and learning, is the mind region affected at first stages of Advertisement, with mind lesions growing with disease development (Tsuiji and Yamanaka, 2014; Ma, 2018). Besides neuronal reduction, Advertisement can be hallmarked from the deposition of extracellular senile plaques pathologically, that have A neurofibrillary and peptides tangles. The later on are constituted by hyperphosphorylated microtubular tau proteins (Nussbaum and Ellis, 2003), as the A peptides within the senile plaques of Advertisement folks are cleavage items from the -amyloid proteins precursor by an organization a proteases, the – namely, -, and -secretases (Hutton et al., 1998). Noticeably, the merchandise from the actions of -secretase certainly are a peptides with 42 proteins size (A42). The A42 is well known because of its pathogenic profile in Advertisement once it really is capable of developing insoluble poisonous fibrils and consequently it accumulates in the special senile plaques of Advertisement (Esler and Wolfe, 2001). Proof LPS and additional gram-negative bacterial fragments co-localizing with amyloid plaques in mind tissue of Advertisement individuals (Zhan et al., 2016; Zhao et al., 2017) shows that microorganisms donate to the excitement of neurodegeneration (Stilling and Cryan, 2016). Therefore, a dual protecting and damaging part of A proteins, categorized as an anti-microbial peptide, continues to be suggested because of its neuroprotective functions (Kumar et al., 2016; Stilling and Cryan, 2016). However, as mentioned previously, aggregation of A protein stimulates the cascade of events occurring during a neuronal proinflammatory response. Therefore, this severe amyloidosis culminates in neurodegeneration (Wang et al., 2015; Kumar et al., 2016; Stilling and Cryan, 2016). A recent study has identified the presence of (is a well-known keystone pathogen in chronic periodontitis. Additional and experiments demonstrated that gingipains are neurotoxic and presented detrimental effects on tau protein. In order to target the neurotoxicity promoted by gingipains, small molecule for its inhibition was designed. The inhibition of these toxic proteases in animal models have revealed to reduce the neuroinflammatory response promoted by gingipains by DKK2 reducing the bacterial load of in the brain, blocked the production of A1C42 and rescued neurons in the hippocampus. Currently, the small molecule is under clinical trials with human subjects (Dominy et al., 2019). Such evidence supports the important role and contribution of host oral and gut microbiotas in AD neurodegeneration (Friedland and Chapman, 2017). Implementation of Metagenomics to Identify an AD Benzocaine Microbiome-Signature and Potential Metabolic Alterations A metagenomics study based on bacterial 16S ribosomal RNA (16S rRNA) gene sequencing of 25 AD diagnosed individuals and 25 asymptomatic age- and sex-matched controls was performed in order to identify gut microbiome alterations in AD. Furthermore, the relationship between the microbiome-signature of AD and its pathology was measured based on well-known cerebrospinal fluid (CSF) biomarkers (Vogt et al., 2017). Alterations Benzocaine in abundance of microbial phyla in AD patients, which included decreases in Firmicutes, Actinobacteria, namely.