Christopher mazaika5/7/2023 ![]() In the first study to examine ICNs using fMRI, reductions in ICN strength were localized to networks involved in attention, language and working memory. A consistent finding across these studies is that individuals with T1DM and comorbid proliferative retinopathy (a marker of microvascular damage) show decreases in functional connectivity relative to individuals with T1DM without retinopathy or age-matched healthy control participants ( 15). Although the physiology underlying ICNs is not completely understood, there is evidence for structural connectivity that underlies ICNs – particularly in the resting state ( 13, 14).Ī growing literature has begun to identify alterations in functional connectivity in individuals with T1DM. These include the salience network, involved in the monitoring of homeostasis and autonomic functioning, the default mode network, a system that tends to be more active in the absence of external stimulation, and the executive control network, involved in cognitive control processes and working memory function ( 12). Regardless of methodology, there are several well-validated and studied ICNs. A recent study utilizing 90 functionally-defined regions of interest identified 14 ICNs that corresponded to a variety of brain functions ( 11). The identification of ICNs can be data-driven, as is done in independent component analysis, or based on regions of interest that have been mapped in previous studies. These fluctuations can be correlated across brain regions to identify intrinsic connectivity networks (ICNs)( 10). not performing an experimental task), brain activity exhibits low frequency fluctuations ( 8, 9). A goal of the present study was to investigate potential differences in functional brain connectivity later in life and to relate these measures to more sensitive measures of structural integrity.įunctional connectivity is a methodology that quantifies the functional associations between brain regions. Moreover, the outcome was measured closer in time to the time of diagnosis, a time when the effects of chronological age on brain integrity are less apparent. Given their use of a less sensitive methodology, it was not possible to identify subtle changes in neuronal integrity or possible alterations in functional connectivity. ![]() Earlier age of onset (defined as < 7 years of age) was associated with increased lateral ventricular volume, as well as poorer performance on measures of psychomotor speed and reasoning ( 7). ![]() To date, the single study to explicitly examine the relationship between age of onset and the brain focused on young adults. For these adults, the brain is not only exposed to the comorbidities of the disease but also the effects of chronological age. What remains unknown is if the associations between age of onset of T1DM in childhood correlate with brain connectivity later in life, particularly for those patients in the fifth and sixth decades of life. A large literature has demonstrated that an earlier age of onset is related to poorer cognitive outcomes, and additional studies have identified relationships between earlier age of onset and microstructural white matter abnormalities in children and young adults ( 6). ![]() Because the metabolic dysregulation associated with T1DM may disrupt normal brain development ( 2– 4), it is not surprising to find evidence of neurocognitive changes in people who develop T1DM in childhood and adolescence, a period when the brain is undergoing dramatic developmental changes ( 5). Mild cognitive dysfunction is a common complication of type 1 diabetes (T1DM)( 1). ![]()
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