Diego A. González-Franco
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Diego A. González-Franco has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Antonio González
Biological and Health Sciences Division, Campus Lerma, Metropolitan Autonomus University (UAM), Lerma 52005, Mexico
1 shared publication - Astrid Gómez
Biological and Health Sciences Division, Campus Lerma, Metropolitan Autonomus University (UAM), Lerma 52005, Mexico
1 shared publication - Gustavo Pacheco-López
Health Sciences Department, Biological and Health Sciences Division, Campus Lerma, Metropolitan Autonomous University (UAM), Lerma 52005 Mexico
1 shared publication - Jaime García-Mena
Departamento de Genética y Biología Molecular, Cinvestav, Av. Instituto Politécnico Nacional 2508, Mexico City 07360, Mexico
1 shared publication - Karina Corona-Cervantes
Tecnológico de Monterrey, Institute for Obesity Research
1 shared publication - Marcel Pérez-Morales
Health Sciences Department, Metropolitan Autonomous University, Campus Lerma, Lerma de Villada, Mexico City 52000, Estado de Mexico, Mexico
1 shared publication
Latest Publications
- Open Access
- 26 July 2022
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 23 (15) , 8209
Chronic-Antibiotics Induced Gut Microbiota Dysbiosis Rescues Memory Impairment and Reduces β-Amyloid Aggregation in a Preclinical Alzheimer’s Disease Model
Alzheimer’s disease (AD) is a multifactorial pathology characterized by β-amyloid (Aβ) deposits, Tau hyperphosphorylation, neuroinflammatory response, and cognitive deficit. Changes in the bacterial gut microbiota (BGM) have been reported as a possible etiological factor of AD. We assessed in offspring (F1) 3xTg, the effect of BGM dysbiosisdysbiosis in mothers (F0) at gestation and F1 from lactation up to the age of 5 months on Aβ and Tau levels in the hippocampus, as well as on spatial memory at the early symptomatic stage of AD. We found that BGM dysbiosisdysbiosis with antibiotics (Abx) treatment in F0 was vertically transferred to their F1 3xTg mice, as observed on postnatal day (PD) 30 and 150. On PD150, we observed a delay in spatial memory impairment and Aβ deposits, but not in Tau and pTau protein in the hippocampus at the early symptomatic stage of AD. These effects are correlated with relative abundance of bacteria and alpha diversity, and are specific to bacterial consortia. Our results suggest that this specific BGM could reduce neuroinflammatory responses related to cerebral amyloidosis and cognitive deficit and activate metabolic pathways associated with the biosynthesis of triggering or protective molecules for AD.
- 26 July 2022
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 23 (15) , 8209
Open AccessChronic-Antibiotics Induced Gut Microbiota Dysbiosis Rescues Memory Impairment and Reduces β-Amyloid Aggregation in a Preclinical Alzheimer’s Disease Model
Alzheimer’s disease (AD) is a multifactorial pathology characterized by β-amyloid (Aβ) deposits, Tau hyperphosphorylation, neuroinflammatory response, and cognitive deficit. Changes in the bacterial gut microbiota (BGM) have been reported as a possible etiological factor of AD. We assessed in offspring (F1) 3xTg, the effect of BGM dysbiosisdysbiosis in mothers (F0) at gestation and F1 from lactation up to the age of 5 months on Aβ and Tau levels in the hippocampus, as well as on spatial memory at the early symptomatic stage of AD. We found that BGM dysbiosisdysbiosis with antibiotics (Abx) treatment in F0 was vertically transferred to their F1 3xTg mice, as observed on postnatal day (PD) 30 and 150. On PD150, we observed a delay in spatial memory impairment and Aβ deposits, but not in Tau and pTau protein in the hippocampus at the early symptomatic stage of AD. These effects are correlated with relative abundance of bacteria and alpha diversity, and are specific to bacterial consortia. Our results suggest that this specific BGM could reduce neuroinflammatory responses related to cerebral amyloidosis and cognitive deficit and activate metabolic pathways associated with the biosynthesis of triggering or protective molecules for AD.