Alzheimer’s Disease in A Petri Dish
Dementia is a major concern for our ageing population, preventing individuals from functioning independently, robbing them of their capacity to reason, communicate with – and even remember – loved ones, and ultimately leading to death. The incidence is expected to double every 20 years, leading to the estimate that by 2050 there will be 115.4 million sufferers, the vast majority of cases being Alzheimer’s disease.
Despite the great and ever increasing impact Alzheimer’s disease has upon the population, the fundamental mechanisms of disease pathology are still uncertain; consequently, no treatments are available for those with the disease. This is not due to negligence on the part of the scientific community; in fact, many years of intensive research have been invested in discerning Alzheimer’s disease pathways. It is not clear why such efforts have not yielded any definitive answers; however, one possibility is the lack of an accurate Alzheimer’s disease model. Due to the nature of the brain, even diagnosing Alzheimer’s disease in living patients proves problematic, thus researchers depend a great deal on disease models. Unfortunately, current Alzheimer’s disease models are not satisfactory; for instance, fruit flies lack the cognitive complexity to carry out sensitive tests on cognition, and rodent models have so far not reproduced the progressive loss of cholinergic neurons from the frontal and temporal lobes that is observed in individuals with late stage Alzheimer’s disease.
Traditionally, cell culture studies of neurodegeneration lead to significant oversimplification, as being restricted to a 2D surface, the neuronal networks formed are much more limited than those of the brain. However, Boston researchers have recently produced a 3D cell model. They used human embryonic stem cells, which were differentiated into neurons, and cultured in a 3D gel, where they formed brain-like connections. The cells were given given genes associated with Alzheimer’s disease, and developed Amyloid-beta plaques and tau tangles; two hallmarks of Alzheimer’s disease. This cell model serially linked these two hallmarks, as drugs that blocked Amyloid-beta prevented formation of tau tangles.
There are still limitations of this cell model, as certain crucial components are absent, such as immune system cells. However, its potential as a tool for high-throughput drug screening, as well as the problems with current animal models, warrants investment. In addition, working with cells avoids the moral quandaries associated with animal studies. Thus, this recent work by Kim and Tanzi is a tremendous boon to the field of Alzheimer’s research, and potentially other neurodegenerative diseases.
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