Medications affect gut microbiome. Bad microbes in the gut can influence the brain and lead to dementia/Alzheimer. As the immune system is affected by medications and gut microbes, the ability of the brain to detox and be free from microbes is influenced by the presence of medications and healthy gut microbes.
There is compelling evidence that the GI microbiome is involved in multiple-related processes such as modulation of circulating hormone levels [12, 13], stimulation of antitumor immune responses [5, 6, 8], and induction of treatment-related toxicities (including immunotherapy-induced colitis [14] and radiation-induced bowel toxicity [15]), and/or morbidities including development of metabolic syndrome [16, 17].
Source: https://www.nature.com/articles/s41391-018-0061-x
A study published by the journal BMJ suggests that benzodiazepine use may promote the development of dementia.
Elderly patients with dementia or Alzheimer’s disease may exhibit increased symptoms of confusion or agitation while taking tramadol.
Other meds that may contribute to dementia include: amitriptyline, paroxetine, and bupropion (most commonly taken for depression) oxybutynin and tolterodine (taken for an overactive bladder) diphenhydramine (a common antihistamine, as found in Benadryl).
A few commonly used non-antibiotic drugs have recently been associated with changes in gut microbiome composition, but the extent of this phenomenon is unknown. We screened >1000 marketed drugs against 40 representative gut bacterial strains, and found that 24% of the drugs with human targets, including members of all therapeutic classes, inhibited the growth of at least one strain. Particular classes such as the chemically diverse antipsychotics were overrepresented. The effects of human-targeted drugs on gut bacteria are reflected on their antibiotic-like side effects in humans and are concordant with existing human cohort studies, providing in vivo relevance for our screen. Susceptibility to antibiotics and human-targeted drugs correlates across bacterial species, suggesting that non-antibiotics may promote antibiotic resistance. Our results provide a comprehensive resource for future research on drug-microbiome interactions, opening new paths for side effect control and drug repurposing, and broaden our view on antibiotic resistance.