Aim Of The Study: To examine the diagnostic utility of skin advanced glycation end products (AGEs) as screening tool of neuropathy in type 2 diabetes mellitus (T2DM).
Patients And Methods: We included 132 participants (88 men) with a mean age of 64.57 years and median T2DM duration of 14.5 years. Skin AGEs were measured with AGE reader mu connect (Diagnoptics) on the dominant arm and were interpreted as normal vs. elevated. Distal sensorimotor polyneuropathy (DSPN) was diagnosed by the Neuropathy Disability Score. Cardiovascular autonomic neuropathy (CAN), sympathetic and parasympathetic nervous system impairment were diagnosed by cardiovascular autonomic reflex tests.
Results: For DSPN, AGEs yielded high sensitivity (82.8%) and NPV (80.4 %) with moderate specificity (55.4 %). For CAN, they yielded relatively high sensitivity (75.0 %) and NPV (74.5 %) with low specificity (48.7 %). For sympathetic nervous system impairment, AGEs yielded relatively high sensitivity (75.0 %) and high NPV (84.3 %) with low specificity (43.9 %). For parasympathetic nervous system impairment, they yielded high PPV (81.0 %) with moderately high sensitivity (66.7 %) and moderate specificity (55.9 %).
Conclusions: In a simplified approach, skin AGEs may be used as a screening tool of DSPN and CAN (including sympathetic and parasympathetic nervous system impairment) in T2DM.
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http://dx.doi.org/10.1016/j.jdiacomp.2022.108356 | DOI Listing |
Chem Sci
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Department of Chemistry, Imperial College London Molecular Sciences Research Hub, 82 Wood Lane, White City Campus London W12 0BZ UK
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Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico.
The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy.
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