ISSN: 2574-8009
Authors: Vincent van Ginneken*
With the increasing aging of the world population, the share in the population with mild Alzheimer's (m-ADs) - also referred to as type-3 diabetes - is increasing. Rough estimates indicate that by 2050 around 140 million people will suffer from this disease, especially in developed countries. m-ADs can be characterized by senile plaques that consist of extracellular amyloid beta (Aβ) deposition while neurofibrillary tangles (NFT) consisting of hyperphosphorylated tau which are located intracellular in Alzheimer Diseased brain. It must be emphasized that these are the consequences of the disease and not the cause. These amyloid plaques have also been observed in other organs of patients with poorly treated type 2 diabetes such as pancreas, liver, kidney and heart, so it must be emphasized that they are not characteristic of the brain alone. But what is then consequently the cause of m-ADs? The idea was first that the brain produced Insulin to a lesser extent but a "breakthrough" study LC-MS by van Ginneken, et al. indicated that in post mortem Type Diabetes brain donors there more saturated bonds occur, making the brain more rigid and the Insulin molecule less likely to reach its destination, leading to neural death. A second hypothesized cause is the formation of plaques in the fluid mosaic membrane of poly unsaturated fatty acids (PUFAs), as a result of which the Insulin molecule is less able to penetrate the human brain, which also leads to neural death. Finally, the role of Sphingomyelins as lipids in foods such as soy and milk should be mentioned, which can be converted via the Land's cycle in the brain to toxic ceramide, which also could lead to neural death. In addition, in a small cohort of patients from the Dutch brain bank - where post mortem histopathological the brain disease has been assessed in addition to body characteristics - it appears that m-ADs or also Type-3 Diabetes is independent of Body Mass Index (BMI).
Keywords: Type-3 Diabetes; Mild-Alzheimer’s Disease; Human Brain; Amyloid Beta (Aβ) Deposition; Amyloid Plaques; Neurofibrillary Tangles (NFT); Type-2 Diabetes; Insulin; Neural Death; Pufas; Sphingomyelins; Ceramide; Food; Body Mass Index (BMI)
