As medical technologies continue to develop, the average human life span is increasing along with them. The world population is getting older on average, a trend that will continue as members of the Baby Boom generation enter their later years. However, as humans live longer and longer, they are more at risk for certain diseases that tend to manifest later in life. One of the diseases we are increasingly susceptible to is Alzheimer’s disease. Alzheimer’s disease is a chronic neurodegenerative disease affecting 48 million people as of 2015; about 6% of people over the age of 65 are affected. It is expected, but not certain, that genetics play a role in the risk of developing Alzheimer’s. The symptoms of the disease usually start out as relatively mild, often manifesting as problems with short-term memory. As the disease progresses, symptoms escalate to include disorientation (Alzheimer’s is responsible for up to 70% of the cases of dementia), loss of motivation, problems with language, poor self-care, mood swings, and behavioral issues. Alzheimer’s is one of the costliest diseases in our society, racking up more than $100 billion annually in charges for treatment such as nursing home care, in-home day care, and indirect costs of locating lost patients and caregiver productivity. There is currently no cure for Alzheimer’s, although treatments such as physical and mental exercise programs may temporarily improve symptoms.
The causes of Alzheimer’s disease are not well understood. The leading theory, accepted by a majority of researchers, is called the “amyloid hypothesis.” This hypothesis is that an accumulation of plaques of amyloid beta (Aβ) proteins in the brain triggers the disease, since these plaques are toxic to nerve cells. The plaques form as Aβ molecules take on a misfolded form. It is possible that misfolded oligomers (known as “seeds”) can cause nearby Aβ proteins to also misfold in a chain reaction very similar to the behavior of prions. Incomplete understanding of exactly how prions work, however, makes the cause of Alzheimer’s even more difficult to pin down.
While the amyloid hypothesis is one of the leading theories regarding the cause of Alzheimer’s, it is not conclusively established. Scientists are still in the process of discovering how Aβ plaques can be treated and how that relates to the progression of the disease. Mice have historically been the animal of choice for studying human genetic diseases, including Alzheimer’s. New research is starting to focus on different ways to attack the disease, such as through the microbiome: how gut bacteria could be linked to the development and progression of Alzheimer’s disease. A recent study focused on looking at how changes in the microbiome of mice could influence the immune system. Specifically, how a constant, long-term antibiotic treatment regime can affect levels of Aβ plaque in the brain. For this study, mice were genetically engineered to have high levels of Aβ plaque in the brain. Some of the mice were fed an antibiotic treatment, while others were not. The researchers monitored the levels of gut bacteria during the study in both groups, as well as the levels of amyloid beta plaque in the brain at the end of the trial. Both groups of mice (with and without antibiotic treatment) had similar levels of gut bacteria throughout the study. However, the mice on antibiotics had a less diverse microbial environment with fewer bacterial species present. Interestingly, this shift in gut bacteria corresponded with a shift in levels of amyloid beta plaque in the mice’s brains, i.e., the mice on antibiotics showed reductions in the Aβ plaque buildup in their brains. The researchers hypothesize that the gut bacteria may influence the levels of immune system molecules (chemokines and cytokines) carried in the blood, and this allows them to affect seemingly unrelated biological systems, like the brain. However, the researchers note that more study is required to fully understand these processes. Also, it is not a given that these results translate to human beings, or that the reduction in amyloid beta plaques in the brain can effectively treat Alzheimer’s. However, this shows that the potential for new treatment vectors does indeed exist that can supplement traditional medical approaches. This study, for instance, shows that methods to attack Aβ plaques directly with medication are also making strides forward.
For experiments like this, involving mice or other rodents, Powers Scientific offers rodent chambers that are adaptable to any environment necessary. Our chambers offer a temperature and lighting controlled environment with a temperature range of 6.5-50°C, and 0-15 fresh air exchanges per hour. Each chamber comes equipped with features such as clock-controlled lighting, solid doors, an interior outlet and access port, doors locks, an audible/visual alarm with relay, stainless steel construction, and casters. Many other options are available, including additional lighting or LED lighting, dual or multi-point temperature control for temperature stressing, top-mounted or remote compressors, extra-deep sizes, or RS-232 or data retransmit outputs. Our chambers are all built to order, allowing the individual researcher to tailor the incubator to fit the required parameters of the experiment without paying for features that aren’t needed.