Abstract
Type-2 diabetes mellitus prevalence is constantly increasing; this is explained by the increase of its risk factors and the amelioration of its management. Therefore, people are living longer with diabetes mellitus, which, in turn, has revealed new complications of the disease. Dementia is represented mainly by Alzheimer's disease and is an interesting topic of study. Accordingly, statistics have shown that dementia incidence is doubled in diabetic patients.The establishment of a relation between type-2 diabetes mellitus was studied on several levels in both humans and animal subjects. First, insulin receptors were found in the brain, especially the hippocampus, and insulin transport to the brain is mainly accomplished through the blood-brain barrier. Secondly, several studies showed that insulin affects multiple neurotransmitters in favor of promoting memory and cognition status. Thirdly, multiple pathological studies showed that insulin and Alzheimer's disease share many common lesions in the brain, such as beta-amyloid plaques, amylin-Aβ plaques, hyper-phosphorylated tau protein, and brain atrophy, especially in the hippocampus. After recognizing the positive effect of insulin on cognitive status, and the harmful effect of insulin resistance on cognitive status, multiple studies were focused on the role of anti-diabetes medications in fighting dementia. Consequently, these studies showed a positive impact of oral anti-diabetes medication, as well as insulin in limiting the progression of dementia and promoting cognitive status. Moreover, their effects were also noticed on limiting the pathological lesions of Alzheimer's disease.Accordingly, we can consider type-2 diabetes mellitus as a risk factor for dementia and Alzheimer's disease. Therefore, this can be used on the pharmaceutical level by the promising implication of antidiabetics as a treatment of dementia and Alzheimer's disease or at least to limit its progression. However, multiple clinical studies should be dedicated to proving the true benefits of anti-diabetes medications in treating dementia before they can be used in reality.
Highlights
BackgroundType-2 diabetes mellitus (T2DM) is featured by chronic resistance to insulin and high blood glucose
Dementia numbers submit to the same equation with a prevalence of 6%-7% in people aged 60 or above [8], along with 46.8 million people living with dementia around the world, with an expected doubling of this number in the two decades according to the 2015 estimate [8]
If we look in the neuron itself, we find that insulin receptors are concentrated in the neuronal soma and even more in the synaptic terminals, which surely, by example if we consider the hippocampus, aid in the function of maintaining memory in it [24,25,26]
Summary
Type-2 diabetes mellitus (T2DM) is featured by chronic resistance to insulin and high blood glucose. Compared to the CSF of normal subjects, a decreased CSF insulin in type-2 diabetes mellitus patients (insulin resistance state) was noticed, which can be explained by decreased transport across the blood-brain barrier [37]. Human-based studies regarding the cognitive decline in type-2 diabetes mellitus patients revealed the following: extremely decreased N-acetylaspartate (NAA) levels, which contribute to altered neuronal integrity, increased myoinositol levels, elevated levels of excitatory neurotransmitters, including glutamate and glycine, and decreased levels of inhibitory neurotransmitters, including GABA which is implicated with pain's perception issues [41]. Alzheimer's disease mice models treated with GLP-1 exerted a neuroprotective effect against apoptosis, oxidative stress, and decreased synaptic plasticity in the hippocampus caused by beta-amyloid [79,80].
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