Alzheimer’s is a deadly disorder (or disease) that eats away at our personhood, but would we ever think it might have some relationship with pickles? Diet has, increasingly, become a focus of our physical and mental health, in terms of the gut-brain axis, our emotions, and neurodegenerative diseases such as ALS and Parkinson’s.
Even as researchers are making some progress in their various hypotheses regarding Alzheimer’s, we are still contending with a very troubling one: it might be an infectious viral disease. But there might only be sporadic instances of this form of SDAT (Senile Dementia of the Alzheimer’s Type). If that’s the case, there may need to be multiple treatment modalities for Alzheimer’s and not one drug. Two broad categories of SDAT have been designated: familial and sporadic, with the latter being poorly understood.
Now, more focus is being placed on factors that were previously thought to be unrelated to AD, such as diet, lifestyle choices, and gut microbiome. Studies have shown that these factors all affect the progression of AD, which raises the possibility that these factors could be key to combating the disease.
Recently, there has been speculation that the gut microbiota-brain axis, a bidirectional communication link between the GI tract and the central nervous system (CNS), may have a role in the etiology and pathogenesis of AD. There may be a link between this axis and the disruption of certain metabolisms or clearances by microbes, the increased permeability of the blood-brain barrier, changes in the neuroinflammatory response, and the blocking of vital hippocampal neurogenesis needed for memory maintenance. These changes in this axis may help explain how AD develops.
Think about how certain foods can alter the gut microbiota, which may lead to changes more in line with the onset of Alzheimer’s. The analysis of the fermented food research has shown promising effects on amyloid-β metabolism, inflammation, and cognitive impairment in animals and humans. The pathogenesis of Alzheimer’s disease emphasizes the role of the gut-brain axis, and studies examining the use of fermented foods are showing promising new research routes. But there’s even more research outside the plumbing of foods and lifestyles.
Globally, the prevalence of mild cognitive impairment, which ranges from 7 % to 25 % in adults aged 60 to 84, continues to increase with advancing age.
Depression, an emotional change seen in Alzheimer’s patients, deserves more attention than it has received in the past. I can remember asking researchers why they weren’t going further in studying depression in these patients. The answer? The patients had depression because of the changes it brought to their lives. Little thought was given to depression as a signaling area of potential research. How might depression, in the biological sense, be involved in this disease? Now that area is opening up to study.
Multiple pathophysiological mechanisms have been proposed to explain the bidirectional relationship between depression and AD. Evidence suggests that midlife depression may be an AD risk factor, while a chronic course of depression in late life may be a sign or symptom of dementia.
There are possible explanations for the possible reciprocal relationship between MCI and depressive symptoms. One is the scarring theory, which holds that depressive episodes make people more vulnerable to cognitive deficits that frequently persist long after affective symptoms have decreased. But, even here, there is a more nuanced approach to both depression and AD and it lies in one hormone, known as the “happiness hormone,” serotonin.
In one study, it was discovered that MCI patients had up to 25% lower serotonin transporter levels in brain regions specifically linked to executive function, emotion, and memory than healthy controls. In addition, the MCI patients had higher levels of plaque material.
Foods that contain preservatives may also play a role in the regulation of serotonin, appetite suppression, and cognition. Sodium benzoate and sodium metabisulfite have the potential to increase serotonin production, which would activate calorie restriction, prolong life expectancy, and improve cognitive performance. Unfortunately, highly processed foods that may contain these two preservatives can bring on other health issues.
Are “happiness” and Alzheimer’s related in some way, as are the foods that aid the gut-microbiota-brain axis in regulating mood and, potentially, Alzheimer’s? The jury is out on this one, but important evidence is being accumulated that may bring new hypotheses and treatments early on in the disease or, potentially, halt it in its tracks. Maybe the lowly pickle will pave the way to a new understanding of fermented foods’ involvement.
