Marco
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My title as the implications go beyong this first paper :
Repurposing Diabetes Drugs for Brain Insulin Resistance in Alzheimer Disease
http://diabetes.diabetesjournals.org/content/63/7/2253.full
This is the full paper so it's long and a bit dense but the gist of it is that there is evidence that Alzheimer pathology may involve dysruption in brain glucose regulation and that AD may be considered a 'type 3' diabetes.
Glucose dysregulation in the brain does not necessary reflect systemic dysregulation beyond the CNS.
Current diabetes meds, particularly those that easily cross the BBB may be repurposed as a treatment (preventative, to slow disease progress and potentially to improve cognition) for AD and possibly other neurodegenerative/neuroinflammatory conditions.
Drugs/biologicals under consideration include intranasal insulin (a current trial is assessing its effects on cognitive impairment in GWS) and leptin (while not an analogue of insulin leptin impacts the same pathways).
On a slightly different but related note, this paper reviews fatigue (physical, reduced activity plus cognitive deficits) in type I and type II diabetes and v controls.
Fatigue and cognitive symptoms in patients with diabetes: Relationship with disease phenotype and
insulin treatment
http://www.psyneuen-journal.com/article/S0306-4530(12)00053-4/fulltext?mobileUi=0
While fatigue and cognitive problems have been variably reported in both types of diabetes, in this study increased physical fatigue and reduced activity compared to controls was found only in type II diabetics while cognitive impairments (reduced processing speed, impaired spatial planning) were found only in insulin treated type II diabetics which was unrelated to diabetes complications such as peripheral neuropathy or to blood glucose control suggesting alternative mechanisms such as adipose tissue induced inflammatory cytokines.
In short impaired insulin metabolism/insulin resistance may be implicated in fatigue, cognitive impairment and cognitive decline in several conditions.
Repurposing Diabetes Drugs for Brain Insulin Resistance in Alzheimer Disease
http://diabetes.diabetesjournals.org/content/63/7/2253.full
This is the full paper so it's long and a bit dense but the gist of it is that there is evidence that Alzheimer pathology may involve dysruption in brain glucose regulation and that AD may be considered a 'type 3' diabetes.
Glucose dysregulation in the brain does not necessary reflect systemic dysregulation beyond the CNS.
Current diabetes meds, particularly those that easily cross the BBB may be repurposed as a treatment (preventative, to slow disease progress and potentially to improve cognition) for AD and possibly other neurodegenerative/neuroinflammatory conditions.
Drugs/biologicals under consideration include intranasal insulin (a current trial is assessing its effects on cognitive impairment in GWS) and leptin (while not an analogue of insulin leptin impacts the same pathways).
On a slightly different but related note, this paper reviews fatigue (physical, reduced activity plus cognitive deficits) in type I and type II diabetes and v controls.
Fatigue and cognitive symptoms in patients with diabetes: Relationship with disease phenotype and
insulin treatment
http://www.psyneuen-journal.com/article/S0306-4530(12)00053-4/fulltext?mobileUi=0
While fatigue and cognitive problems have been variably reported in both types of diabetes, in this study increased physical fatigue and reduced activity compared to controls was found only in type II diabetics while cognitive impairments (reduced processing speed, impaired spatial planning) were found only in insulin treated type II diabetics which was unrelated to diabetes complications such as peripheral neuropathy or to blood glucose control suggesting alternative mechanisms such as adipose tissue induced inflammatory cytokines.
In short impaired insulin metabolism/insulin resistance may be implicated in fatigue, cognitive impairment and cognitive decline in several conditions.