Potential benefits of kefir and its compounds on Alzheimer's disease: A systematic review

Abstract

Alzheimer's disease, characterized by the progressive loss of cognitive functions of the brain, is still an incurable pathology. Current treatments primarily aim to alleviate symptoms, acting mainly on behavioral changes, having a modest impact in the disease course. Recently, potential role of probiotics in managing Alzheimer's has been explored. Kefir, a fermented food teeming with live microorganisms, is thought to influence the gut microbiota, potentially reducing inflammation and the accumulation of toxic proteins in the brain. Additionally, kefir contains bioactive compounds, such as B vitamins, choline, and folic acid, which are essential for neuronal health and cognitive function. Thus, kefir could emerge as a promising complementary treatment for Alzheimer's disease. This systematic review, conducted in January 2024, examined the effects of kefir in both in vivo animal models and human patients with neurodegenerative conditions. The review was based on studies retrieved from BVS, Embase, PubMed/MEDLINE, Scopus, and Web of Science databases. Seven studies were included, involving invertebrates, murine models, and human participants. In animal models, the primary outcomes were antioxidant effects, reduced beta-amyloid deposition, and attenuation of vascular damage and neurodegeneration. In human studies, kefir supplementation resulted in decreased levels of inflammatory cytokines, reactive oxygen species (ROS), and oxidative proteins, and was associated with improvements in memory. Given its potential benefits, kefir could serve as a valuable adjunct to conventional treatments for Alzheimer's disease, warranting further investigation in clinical settings.

Keywords: Fermented milk; Kefir; Neurodegenerative diseases and Alzheimer.

Fig. 1

Flowchart of the kefir and Alzheimer's disease articles selection for systematic review and meta-analysis according to PRISMA criteria.

Fig. 2

This figure illustrates the role of intestinal dysbiosis in neuroinflammation and the pathophysiology of Alzheimer's disease. Dysbiotic gut microbiota activates inflammatory pathways, leading to increased oxidative stress. This, in turn, triggers microglial activation in the central nervous system. Activated microglia then stimulate astrocytes, resulting in the disruption of the blood-brain barrier (BBB), which further perpetuates microglial activation in a vicious cycle. Both BBB compromise and microglial activation contribute to the formation and deposition of beta-amyloid plaques and neurofibrillary tangles, through hyperphosphorylation of tau protein, which promote neuronal apoptosis, synaptic dysfunction, and disease progression. Created in https://BioRender.com.

Fig. 3

Fig. 2: GALT= Gut-associated lymphoid tissue. The figure illustrates the central role of the gut microbiota in human health through interconnected functions. It regulates the immune system by promoting tolerance to non-pathogenic stimuli and competing with pathogens. The microbiota affects the gut-brain axis through bidirectional nerve communication and bloodstream transport of bacterial metabolites, toxins, and fragments, influencing brain function and inflammation. It aids in metabolism by producing short-chain fatty acids, converting bile acids, and synthesizing digestive enzymes, while contributing to vitamin production. A healthy microbiota maintains the intestinal barrier, preventing harmful bacterial byproducts translocation to the bloodstream and protecting systemic and neurological health (LeBlanc et al., 2013). Created in https://BioRender.com.