BACKGROUND: Parkinson’s disease is a chronic neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. We found a marked relationship between diabetes and memory, as just over half of the patients (52%) had below-average scores on the WMS. There is increasing evidence that risk factors for metabolic syndrome (such as prediabetes) increase risk of incident cognitive impairment and possibly AD, and evidence that the neurons of the AD brain are in fact insulin resistant with diminished glucose uptake under physiological conditions. Interestingly, in contrast to non-diabetic mice, such a short transient cerebral ischemia significantly impaired cognitive function and caused brain atrophy in diabetic mice. Understanding the predisposing factors and the link between diabetes and CI or dementia can help improve the quality of life of diabetic individuals. Prospective analyses: no association of baseline history of hypoglycemia and risk of ‘cognitive decline’ in patients free of cognitive impairment at baseline (unadjusted). 28.31±2.24, P-value=0.000).
Carriers of this allele who also have type 2 diabetes have a two-fold increased risk of developing Alzheimer’s disease compared to those who have the allele but not diabetes. We may discovery the unrevealed mechanism for the divergent between IR and diabetes group. Taken together, our findings suggest that nifedipine ameliorates impaired cognitive function in type 2 diabetic mice, at least because of attenuation of hyperinsulinemia and superoxide production in the brain and possible upregulation of the neural differentiation-controlling gene, Id-1. Although a history of hypoglycemic events was not a predictor of cognitive impairment, we cannot exclude the possibility that the influence of young age of diabetes onset depends on the effect of hypoglycemic events early in life. Although type 2 diabetes accelerates age-related cognitive decline, younger patients also show signs of cognitive impairment. In current study, we take cerebral ventricle volume, which may represent the structure changes of the whole brain, as a covariant. We have demonstrated that diabetes and pre-diabetes increase the risk of dementia and its main subtypes (5,18–20).
Imaging reports of this respect in diabetes are limited. We undergo the examination of DKI, instead of DTI to explore the real world of microstructure. A critical event downstream of glutamate receptor activation is poly(ADP-ribose) polymerase-1 (PARP-1) activation (4). Most of them are studies of one or two protocols. In our study, multi-modal sequences will be conducted and analyzed at the same time. Loss of cognitive function was calculated by subtracting CCF from PCF. Corresponding sensitivity and specificity are calculated, and then we will get the cutoff values to diagnose MCI.
MoCA is verified to be a valid scale for MCI in diabetes in China . The aim of this investigation is to reveal the relationship between diabetes mellitus type 2 and cognitive impairment. Therefore, we may detect the functional node for different cognitive dimensions. Performance in cognitive tests also was reduced in T2DM patients and this was associated with reduced ReHo and ALFF values in the cuneus and lingual gyrus, regions associated with visual memory and word processing (16). The neuropsychological test battery comprises another four scales. They test the condition of cognition, affection and life style. Different cognitive-related circuits overlap and interact significantly.
A randomized control study and several case reports suggest that GADA-associated neurological manifestations are reversible and are successfully treated by immunomodulating therapy [36, 37]. Treatment strategies vary significantly. According to our preliminary experiment, patients took metformin either alone or in combination with other drugs. Some of the diabetes went on insulin treatment. Part of the prediabetes group took statin-related drugs. Antihypertensive drugs were also taken by some individuals to control their blood pressure. Medications related to cardiovascular disease affect cerebral perfusion significantly , and they may play a role in neuronal plasticity as well .
In the current study, we have not taken medication therapies as covariant for some practice and ethics issues. The reliability of results may be affected by the disaccord of medication therapies. Future studies should focus on comparing the imaging characteristics between MCI converted group and no converted group. Gene type may serve as a control condition. Other techniques such as using MRS for the metabolic data could be useful and should be evaluated as well. The consistency of therapeutic regimen should also be guaranteed.