Research into the molecular nature of Alzheimer’s Disease has been a major focus the past 20 years, with (AD) claiming about 90,000 Americans annually. With genetic factors attributing to AD very minimal, the mechanisms of sporadic, late-onset AD is still not fully clarified. Intense research efforts have sought to identify this complex neurological disorder the past few years.
Recent research has unveiled the connection between Alzheimer’s disease and Insulin signaling, indicating a brain-specific form of diabetes. Several clinical studies have now established factors including hyperglycemia and hyperinsulinemia has correlated positively with the development of Alzheimer’s development in humans. Overall, Alzheimer’s brains have exhibited malfunctioning insulin pathways, and a largely decreased responsiveness to insulin.
After years of belief that insulin has no belonging in the brain, numerous studies have revealed insulin actions are key for
neuronal survival and brain function. It is now established insulin regulates brain metabolism and energy balance in the hypothalamus, and is important for memory formation, association, and retrieval in the forebrain and hippocampus. Other functions include having neuroprotective properties and having a large role in cognitive functioning.
For the last 15 years, Alzheimer’s disease has been distinguished by a few specific characteristics: senile plaques and neurological tangles. Senile plagues are composed of large clumps of amyloid fibrils, specifically amyloid-β (Aβ) peptides. However despite a proven toxicity of these large aggregates, many post-mortem observations showed that the large amyloid plagues did not correlate well with AD symptoms. Instead, a loss in plasticity or neuronal signaling was discovered to be associated with oligomers of Aβ peptides called AβO’s. These toxins are now considered responsible for synapse loss and triggering Alzheimer’s Disease symptoms.
In conditions such as type 2 diabetes, sustained metabolic stress and inflammatory signaling lead to decreased insulin signaling and a decreased biological response to insulin. This is called insulin resistance, and this significantly impairs your body to properly store energy in your blood, so characteristically glucose levels soar through the roof with diabetes patients. Interestingly, this same process occurs in the brain with insulin signaling in the occurrence of Alzheimer’s disease. Several recent studies have linked neuropathic mechanisms triggered by AβOs to mechanisms involved in insulin resistance in diabetes.
Overall, if AD mechanisms are from the same causation as type 2 diabetes, these conditions can be prevented from occurring through maintaining a healthy lifestyle. The most important factor in preventing diabetes, and eventually Alzheimer’s disease, is limiting your amount of body fat. Developing excess weight near your abdomen has been closely linked to insulin resistance. This is because this deep fat isn’t near your skin, and is more likely to cause insulin resistance compared to fat developed on your hips and thighs.
Eating a diet of high-fiber, slow-release carbohydrates is an important step in a healthy diet. Carbohydrates have a big impact on your blood sugar levels, so having a smart approach to what types of carbohydrates you eat is important. Complex carbohydrates include foods like brown ride, whole-wheat pasta, whole-wheat foods, high-fiber cereals, peas and leafy greens.
Overall, several studies have shown a link of insulin resistance to the increasingly common Alzheimer’s disease. Insulin resistance has shown to have little genetic connections, so a healthy lifestyle and diet are key controllable aspects that will ultimately decrease your chances of Alzheimer’s disease.
