Type 2 Diabetes Mellitus can cause a quote “leaky brain”…
…which in turn can increases risk of:
- Cognitive decline
- Alzheimer’s disease
Cardiovasc Psychiatry Neurol. 2011 Published online 2011 February 17
Vascular Pathology and Blood-Brain Barrier Disruption in Cognitive and Psychiatric Complications of Type 2 Diabetes Mellitus
Vascular pathology is recognized as a principle insult in type 2 diabetes mellitus (T2DM).
Co-morbidities such as structural brain abnormalities, cognitive, learning and memory deficits are also prevailing in T2DM patients.
We previously suggested that microvascular pathologies involving blood-brain barrier (BBB) breakdown results in leakage of serum-derived components into the brain parenchyma, leading to neuronal dysfunction manifested as psychiatric illnesses.
The current postulate focuses on the molecular mechanisms controlling BBB permeability in T2DM, as key contributors to the pathogenesis of mental disorders in patients.
Revealing the mechanisms underlying BBB dysfunction and inflammatory response in T2DM and their role in metabolic disturbances, abnormal neurovascular coupling and neuronal plasticity, would contribute to the understanding of the mechanisms underlying psychopathologies in diabetic patients.
Establishing this link would offer new targets for future therapeutic interventions.
Link to the full article on Pub Med: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042607/?tool=pubmed
Inflammation and vascular pathology have a significant contribution for the pathogenesis of T2DM complications.
Neuropsychiatric disorders are also associated with inflammatory reaction and cerebrovascular impairments.
Brain injuries that often involve Blood Brain Barrier breakdown and astrocytic response increase the risk for neuropsychiatric sequelae, including personality changes, depression, anxiety, dementia, and perhaps psychosis.
T2DM patients show higher susceptibility to cerebrovascular diseases which according to our hypothesis may explain the increased incidence of cognitive deterioration, depression, vascular dementia, lacunar infarcts, hemorrhages and Alzheimer’s disease among these patients.
Revealing the mechanisms underlying the effects of diabetes on BBB structure and function and understanding the role of inflammation, impaired neurovascular coupling, metabolic defects and altered neuronal plasticity in the neuropsychiatric sequela of T2DM, will create a target for clinical and pharmacologic modalities and a potential platform for future therapeutic intervention.
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