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Insulin could play a part in reversing Alzheimer’s symptom

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Photo courtesy hudsonvalleynewsnetwork.com.

Photo courtesy hudsonvalleynewsnetwork.com.

Photo courtesy hudsonvalleynewsnetwork.com.

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With its creeping, irreversible symptoms, Alzheimer’s Disease (AD) is terrifying and devastating. Yet with recent advances in biomedical research, there is emerging hope that this disease, with its insidious effects on quality of life, may be treatable.

AD is a multi-faceted, complicated disease involving higher cognitive functions, making it difficult to model in lab animals. However, some of the simpler characteristics of AD — including impaired memory and physical damage to the brain — can be replicated by injecting streptozocin (STZ), a toxic look-alike of glucose, into the brains of animal models.

STZ is known to kill off cells that sense glucose levels in the brain, and because the brain is almost entirely dependent on glucose for energy, administering STZ directly into the brain can effectively mimic the brain glucose imbalance found in AD (Deng et al.). This disruption of the glucose balance results in the decrease of protective processes and an increase of dangerous protein accumulation. Most AD researchers especially focus on two of the key hallmarks of AD when studying animal models. These are the increase in abnormal tau protein (which, when healthy, serve to stabilize neurons in the brain) and the destruction of normal electrical signaling junctions (synapses). STZ, by offsetting the glucose balance in the brain, causes these symptoms to develop, allowing for a fairly accurate and widely used AD animal model.

Because the balance of glucose in the brain is critical to preventing the onset of AD symptoms, insulin — a widely recognized signaling hormone associated with glucose uptake — likely plays a central role in maintaining a healthy brain in aging individuals. With this hypothesis in mind, researchers Guo and Chen et al. hypothesized that restoring normal insulin levels in the brains of AD mouse models could reverse some of the cognitive and physical symptoms of AD. They therefore conducted a study on the effects of intranasally delivered insulin on the symptoms of AD in rat models. In this study, rat models with characteristic AD symptoms induced by STZ were given intranasal insulin for six weeks, and were then compared to normal rats and rats with STZ-induced AD that did not receive the insulin. The intranasal delivery method was used because it would bypass the blood-brain barrier, which prevents intravenously injected insulin from reaching the brain.

After six weeks, the researchers subjected the rats to a water maze test, where the rats had to find and swim to the location of a platform under the surface of the water.  This is the standard approach to test short-term learning and memory in rodents, since daily repetition of the test enables animals with intact memory to more easily find the platform each time they repeat it. The researcher found that rats with AD had difficulty identifying the location of the platform upon repetition of the test. This indicated a significant loss of spatial memory. However, the AD rats that had received insulin demonstrated behavior almost identical to the control rats, indicating a recovery of the spatial memory loss induced by AD.

In addition to testing the behavioral aspect of AD, the researchers also explored the capacity of insulin to reverse some of the physical symptoms of AD. Specifically, they looked at the impact of insulin on the two key hallmarks of AD noted above: tau aggregation and the destruction of synapses. By extracted and analyzing the brains of the rats, the researchers found that tau function was normal in insulin-treated AD rats, despite the non-treated AD rats displaying dramatically increased levels of tau dysfunction. This indicated that insulin may be reversing some of the pre-existing physical damage to the brain, and could be a cause of the restored memory in the treated AD rats. Additionally, the researchers found that the amount of neuron and synapse regeneration was significantly higher after insulin treatment versus without, lending more support to the notion that intranasal insulin was restoring brain function by physical restoration of the brain.

While this model does not completely encompass the entirety of AD, many of the main characteristics of the disease were alleviated or reversed in this study. The potential of insulin — a readily available therapeutic — to reverse AD symptoms gives reason to hope that the slow and ominous progression of AD symptoms could be alleviated by a relatively simple treatment paradigm in the near future.

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