Gut microbiome changes improve memory in early cognitive decline

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Gut microbiome changes improve memory in early cognitive decline

From Mediterranean diets to probiotics, scientists reveal how reshaping the gut microbiome could help protect brain function, while highlighting why timing may be critical for slowing cognitive decline. 

Study: The association between gut microbiota and cognitive decline: A systematic review of the literature. Image credit: Toa55/Shutterstock.com

The gut-brain axis is gaining importance as a modulator of brain functional health. A recent paper in Nutrition Research synthesized evidence from the literature to show that multiple approaches to manipulating the gut microbiome share common biological pathways to improve cognitive performance in adults aged 45 years or older with cognitive impairment or at risk of dementia.

Aging gut microbiota shifts linked to dementia risk 

Multiple neurodegenerative disorders like Alzheimer’s disease (AD) are mediated in part by alterations in the gut-brain axis caused by aging-related shifts in the gut microbiota. Dementia is progressive and irreversible, causing neurological decline and a reduced life expectancy.

This is in contrast to the early stages of cognitive impairment, or mild cognitive impairment (MCI), when functional deficits can be detected but typically do not affect daily functioning.

Gut-brain mechanisms underlying cognitive decline

The gut-brain axis is a bidirectional communication system between the central nervous system and the gut. It involves signaling via nerves, hormones, and immunological mediators. Recent research has established its important role in regulating neurodevelopment, mood, and cognition.

However, age- and diet-related changes in the gut microbiota may induce dysbiosis, which is thought to contribute to the onset of neurodegeneration.

With gut dysbiosis, the gut epithelial barrier is compromised. This allows bacteria and microbial-associated molecular patterns to enter the bloodstream. The resulting systemic endotoxemia may trigger chronic low-grade inflammation. Gut dysbiosis also causes immune cell abnormalities, resulting in a systemic pro-inflammatory state.

Systemic inflammation may weaken the blood-brain barrier (BBB), exposing the brain to pro-inflammatory triggers and mediators. The resulting neuroinflammation is associated with the accumulation of abnormal proteins, such as amyloid-β and tau, the hallmark of AD. Neuronal synapses are damaged, and function is impaired. The eventual outcome is cognitive decline, whether as a part of aging or of AD.

The microbiome, immune system, and brain are engaged in a continuous dialogue, where perturbations in one component can reverberate throughout the system, creating a vicious cycle that promotes cognitive decline.

Microbiome research evolves from observation to intervention

The researchers outlined the progression of such studies. The earliest, purely descriptive, studies of gut microbial responses were followed by detailed microbiome characterizations driven by advances in DNA and RNA sequencing and metabolomics. This was followed by the current interventional studies with a stronger mechanistic focus.

Integrating evidence on dysbiosis and cognition

The authors aimed to pull together evidence from studies covering various microbiota-targeting interventions in isolation. They reviewed the literature on cognitive changes in adults aged 45 years or older with cognitive impairment or at risk of dementia who participated in experimental manipulations of the gut microbiota.

The interventions included probiotics, prebiotics, methyl donor nutrient supplementation, omega-3 fatty acid intake, synbiotics, fecal microbiota transplants (FMT), and diets like the Mediterranean or keto diets. The patients were evaluated for inflammatory and metabolic changes, as well as alterations in fecal microbiota.

Microbiota changes linked to cognitive improvement

The review included 15 studies covering a range of demographic characteristics. The study sample ranged from 5 to over 1,200 participants. Overall, there were 4,275 participants.