Abstract
Alzheimer’s disease (AD) is the most common cause of dementia. Epidemiological studies show the association between AD and type 2 diabetes (T2DM), although the mechanisms are not fully understood. Dietary habits and lifestyle, that are risk factors in both diseases, strongly modulate gut microbiota composition. Also, the brain-gut axis plays a relevant role in AD, diabetes and inflammation, through products of bacterial metabolism, like short-chain fatty acids. We provide a comprehensive review of current literature on the relation between dysbiosis, altered inflammatory cytokines profile and microglia in preclinical models of AD, T2DM and models that reproduce both diseases as commonly observed in the clinic. Increased proinflammatory cytokines, such as IL-1β and TNF-α, are widely detected. Microbiome analysis shows alterations in Actinobacteria, Bacteroidetes or Firmicutes phyla, among others. Altered α- and β-diversity is observed in mice depending on genotype, gender and age; therefore, alterations in bacteria taxa highly depend on the models and approaches. We also review the use of pre- and probiotic supplements, that by favoring a healthy microbiome ameliorate AD and T2DM pathologies. Whereas extensive studies have been carried out, further research would be necessary to fully understand the relation between diet, microbiome and inflammation in AD and T2DM.
Highlights
Division of Physiology, School of Medicine, Universidad de Cadiz, 11003 Cadiz, Spain; Instituto de Investigacion e Innovacion en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Salus Infirmorum, Universidad de Cadiz, 11005 Cadiz, Spain
Previous studies have reported lower bacterial diversity and more similar bacteria composition when young Alzheimer’s disease (AD) mice are compared with wildtype counterparts [90,107,132], while further differences are shown as the age of the animals increase [90]
Previous studies suggest that AD and T2DM pathologies can improve through the treatment of pre-and probiotics [87,151,152,153,248,258], caloric restriction diets [27,157,207,220] or antioxidants [154], helping to regulate intestinal dysbiosis and reduce the inflammation
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Apart from classical neuropathological features of AD, other alterations have been described, and the concept of neurodegeneration has expanded to accommodate early alterations that include oxidative stress or inflammation [9] Following this idea, neuroinflammation plays a significant role in neurodegeneration [10]. On the other hand, growing evidence has shown that alterations in the gut microbiota composition can alter normal brain function through the so-called gut–brain axis. Following this idea, the bidirectional communication between the central nervous system (CNS) and the gastrointestinal tract plays a key role in the pathogenesis of a variety of neuropsychiatric disorders and AD [17]. In opposite direction, AD pathology could affect gut microbiota composition [17,19]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call