Alzheimer’s disease is a thief.

First it takes your car keys, friends’ names, ability to feed yourself, get dressed and then even recognition of beloved family faces until your brain is a blank slate. Your entire memory is wiped clean just when you want to revisit the best of your life.

Faltering minds may have a new ally in microbes. Alzheimer’s disease, characterized by abnormal protein clumping in the brain, is a prime target. Why?

Aging brings less diversity in microbes. Microbes change too in composition, structure and function. That may be bad because gut microbes greatly impact the brain and behavior and may be involved in critical phases of neurodevelopment and neurodegenerative disorders such as Alzheimer’s.

Take a minute for an update.

To the delight of neuroscientists, the gut-brain axis is no longer the road less travelled. The vagus nerve acts as traffic cop; it mediates gut communication with the brain and then the flow in the opposite direction. All sorts of activity rule the road: intestinal motility, gut and brain immune response, neurotransmitter release, and transfer of metabolites including short-chain fatty acids and dietary amino acids catabolites.  These mediators travel into the brain and help activate immune cells called microglia which in addition to fighting off invaders, prune unwieldy synapses and clear out debris. Without them the mind wilts.

Of course, brain science IS like rocket science. For an excellent dive into the arcane, refer to Of Microbes and Minds: A Narrative Review on the Second Brain Aging published by Italian researchers in March of 2018 in Frontiers in Medicine.

Aging changes the brain and entire body that extends to the gut-brain axis. A host of problems ensue:

• Increased gut permeability
• Reduced gut microbial richness and diversity
• Hypothalamic–pituitary–adrenal axis (HPA) is deeply disturbed.
• Sleep disruption is implicated in gut dysbiosis.
• The synthesis of neurotrophic factors and neurotransmitters suffers.
• Decline in immune function (immunosenescence) associated with a chronic, low-grade inflammation (inflamm-aging) leads to brain changes.

The authors detail how microbes may figure in neurological diseases such as Alzheimer’s:

• Gut microbiota may program the activity of multiple neurotransmitter systems in different brain regions.
• The gut microbiota may also play a role in synapse maturation and synaptogenesis.
• The blood-brain barrier begins construction in the womb; dysbiosis then can cause life-long permeability, leading to pathogen invasion.
• Microbiota alterations (via antibiotics, prebiotic and probiotic use) can affect microglia in the short and long-term. For example, mice treated with antibiotics showed decreased hippocampal neurogenesis and memory retention.

Thus changing the gut microbes may attack brain dysfunction from many different angles.

Most initial evidence of the gut microbe link is from animal studies. For example, a trial of lactic acid bacteria and bifidobacteria improved cognitive function as well as a slew of other biomarkers noted on a healthy gut-brain axis.

Animal studies are a start. Threads linking brain function and gut microbes are rich in possibility. For something as devastating as Alzheimer’s disease, rigorous clinical trials in humans are urgent.