Cognitive decline is one of the major causes of disability in older people. A high level of homocysteine, a byproduct of vitamin B, has been linked to brain atrophy, which itself is a precursor to cognitive decline leading to dementia and Alzheimer's disease. In addition, a low level of vitamin B is often noted in patients with dementia and Alzheimer's disease and its supplementation has been shown to improve memory and to slow the progress of brain atrophy. This information may aid in the use of vitamin B as a preventative measure against severe cognitive decline, and thus reduce the onset of conditions such as dementia and Alzheimer's disease.

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder that falls under the umbrella of dementia and is characterised by the presence of highly neurotoxic amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) of tau protein within the brain. Historically, treatments for AD have consisted of medications that can slow the progression of symptoms but not halt or reverse them. The shortcomings of conventional drugs have led to a growing need for novel, effective approaches to the treatment of AD. In recent years, immunotherapies have been at the forefront of these efforts. Briefly, immunotherapies utilise the immune system of the patient to treat a condition, with common immunotherapies for AD consisting of the use of monoclonal antibodies or vaccines. Most of these treatments target the production and deposition of Aβ due to its neurotoxicity, but treatments specifically targeting tau protein are being researched as well. These treatments have had great variance in their efficacy and safety, leading to a constant need for the research and development of new safe and effective treatments.

Methamphetamine (METH) is a highly addictive drug abused by millions of users worldwide, thus becoming a global health concern with limited management options. The inefficiency of existing treatment methods has driven research into understanding the mechanisms underlying METH-induced disorders and finding effective treatments. This study aims to understand the complex interactions of the gastrointestinal–immune–nervous systems following an acute METH dose administration as one of the potential underlying molecular mechanisms concentrating on the impact of METH abuse on gut permeability. Findings showed a decreased expression of tight junction proteins ZO-1 and EpCAm in intestinal tissue and the presence of FABP-1 in sera of METH treated mice suggests intestinal wall disruption. The increased presence of CD45+ immune cells in the intestinal wall further confirms gut wall inflammation/disruption. In the brain, the expression of inflammatory markers Ccl2, Cxcl1, IL-1β, TMEM119, and the presence of albumin were higher in METH mice compared to shams, suggesting METH-induced blood–brain barrier disruption. In the spleen, cellular and gene changes are also noted. In addition, mice treated with an acute dose of METH showed anxious behavior in dark and light, open field, and elevated maze tests compared to sham controls. The findings on METH-induced inflammation and anxiety may provide opportunities to develop effective treatments for METH addiction in the future.