fbpx Prevention of type-1 diabetes induced neurocognitive deficits by modulating the plasticity of cerebrovascular function: a pilot | HMRI

The knock-on effects are poorer intellectual performance, low job complexity in adulthood and loss of the cognitive reserve that protects against dementia in old age. In fact, compared to non-diabetics, elderly adults with T1D are 83% more likely to get dementia, compared to a 50% greater risk in T2D. Thus more vigilance is needed to address cognitive changes in people with T1D as they age, yet very little research has been done to examine the underlying mechanisms by which T1D impacts cognitive function throughout life. 

The consequences of diabetes differ between types. T1D adults have greater risk of blindness resulting from damage to small vessels in the retina. This suggests that the microvessels in the brain are also likely to be damaged from early exposure to high blood glucose levels. Together with the low level chronic inflammation associated with T1D, vessels become stiff and lose elasticity, which reduces blood flow to neurons during mental activity which can impact cognitive functioning. We have shown that older adults with T2D have poorer cognitive function compared to non-diabetes that is accompanied by increased cerebral artery stiffness and reduced perfusion in the brain. No studies have characterised this mechanistic link in T1D. We believe that adults with T1D also have impaired blood vessel function in the brain, which is in turn compromises their cognitive function.  

This pilot project aims to characterise the extent to which poor vessel function in the brain is contributing to cognitive deficits in adults with T1D. Using non-invasive transcranial Doppler ultrasound to determine the magnitude of increase in blood flow velocity in the brain while performing a mental task, we can indirectly ascertain the relationship between the vasodilator capacity of the vessels and performance on the mental task. We have consistently shown the robustness and sensitivity of this unique technique to detect improvements in vessel health to various non-pharmacological interventions. We will also determine the contribution of disease duration, metabolic status, glycaemic fluctuations and inflammation on brain function. 

Outcomes of this cross-sectional investigation will indicate whether T1D adults should have their cognitive function tested starting in their 40s and 50s as part of their on-going diabetes management plan. Further, the study findings will provide scope for future investigation of therapeutic strategies that have been shown to restore cerebral vascular function and attenuate cognitive decline in young T1D and in adult patients at-risk for dementia.


Dr Rachel Wong, Dr Ryu Takechi, Prof Peter Howe, Dr Matthew Albrecht

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