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Brain Insulin Resistance Identified As Possible New Link Between Alzheimer's Disease, Diabetes

paymanz

Member
Joined
Jan 6, 2015
Messages
2,697
It says brains inability to burn glucose is responsible for Alzheimer's disease.caused by insulin's resistance in brain, and that probably mediated by inflammation.

Brain Insulin Resistance Contributes to Cognitive Decline in Alzheimer's Disease – PR News

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The risk of developing Alzheimer's disease is increased by 50 percent in people with diabetes. Type 2 diabetes is due to insulin resistance and accounts for 90 percent of all diabetes cases. The defining clinical feature of Type 2 diabetes (and Type 1 "juvenile" diabetes) is hyperglycemia — high levels of sugar in the blood - but there is no evidence that the brain in Alzheimer's is hyperglycemic. Nevertheless, insulin resistance in tissues outside the brain with or without hyperglycemia can potentially cause insulin resistance in the brain and thereby contribute to the onset of Alzheimer's disease. "The new research demonstrates not only that the brain in Alzheimer's disease is, in fact, insulin resistant, but that this occurs in non-diabetics and hence in the absence of hyperglycemia outside the brain,"

https://www.hindawi.com/journals/mi/2015/105828/

Type 2 diabetes (T2DM), Alzheimer’s disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer’s disease (AD) is the most common subtype of dementia. Reduced release (for T2DM) and decreased action of insulin are central to the development and progression of both T2DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T2DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic inflammatory response and oxidative stress associated with T2DM, amyloid-β (Aβ) protein accumulation, and mitochondrial dysfunction link T2DM and AD.

http://www.sciencedirect.com/science/article/pii/S155252601302918X

Compelling preclinical and clinical evidence supports a pathophysiological connection between Alzheimer's disease (AD) and diabetes. Altered metabolism, inflammation, and insulin resistance are key pathological features of both diseases. For many years, it was generally considered that the brain was insensitive to insulin, but it is now accepted that this hormone has central neuromodulatory functions, including roles in learning and memory, that are impaired in AD. However, until recently, the molecular mechanisms accounting for brain insulin resistance in AD have remained elusive. Here, we review recent evidence that sheds light on how brain insulin dysfunction is initiated at a molecular level and why abnormal insulin signaling culminates in synaptic failure and memory decline. We also discuss the cellular basis underlying the beneficial effects of stimulation of brain insulin signaling on cognition. Discoveries summarized here provide pathophysiological background for identification of novel molecular targets and for development of alternative therapeutic approaches in AD

Recent evidence indicates that AD is a brain-specific form of diabetes
.........Moreover, AD brains exhibit defective insulin signaling, altered levels and/or aberrant activation of components of the insulin signaling pathway, and, more importantly, decreased responsiveness to insulin...........
Although the brain was once considered an insulin-insensitive organ, and the source of brain-acting insulin is still a matter of debate [16], it is now established that insulin actions are important for neuronal survival and brain function
........
In type 2 diabetes, aberrant tumor necrosis factor-α (TNF-α) signaling leads to activation of the stress kinase c-Jun N-terminal kinase (JNK) [48]. Activated JNK phosphorylates IRS-1 at serine residues (IRS-1pSer), blocking downstream insulin signaling and causing peripheral insulin resistance [40]. Similarly, it was shown recently that AβOs instigate aberrant activation of the TNF-α/JNK pathway and IRS-1 inhibition in primary hippocampal neurons [41] and [44], and in the hippocampi of cynomolgus monkeys that received intracerebroventricular infusions of AβOs [41]. IRS-1 inhibition was also demonstrated in the brains of a transgenic mouse model of AD [41]. Most important in establishing the clinical relevance of these findings was the demonstration of elevated IRS-1pSer [14] and [41] and activated JNK [41] in postmortem AD brains.
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Blocking Inflammation From PUFA Reverses Brain Aging

JNK And Tumor Necrosis Factor-alpha Mediate Free Fatty Acid-induced Insulin Resistance In 3T3-L1 Adi
 

Koveras

Member
Joined
Dec 17, 2015
Messages
719
It says brains inability to burn glucose is responsible for Alzheimer's disease.caused by insulin's resistance in brain, and that probably mediated by inflammation.

Brain Insulin Resistance Contributes to Cognitive Decline in Alzheimer's Disease – PR News



https://www.hindawi.com/journals/mi/2015/105828/

Type 2 diabetes (T2DM), Alzheimer’s disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer’s disease (AD) is the most common subtype of dementia. Reduced release (for T2DM) and decreased action of insulin are central to the development and progression of both T2DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T2DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic inflammatory response and oxidative stress associated with T2DM, amyloid-β (Aβ) protein accumulation, and mitochondrial dysfunction link T2DM and AD.

http://www.sciencedirect.com/science/article/pii/S155252601302918X

Compelling preclinical and clinical evidence supports a pathophysiological connection between Alzheimer's disease (AD) and diabetes. Altered metabolism, inflammation, and insulin resistance are key pathological features of both diseases. For many years, it was generally considered that the brain was insensitive to insulin, but it is now accepted that this hormone has central neuromodulatory functions, including roles in learning and memory, that are impaired in AD. However, until recently, the molecular mechanisms accounting for brain insulin resistance in AD have remained elusive. Here, we review recent evidence that sheds light on how brain insulin dysfunction is initiated at a molecular level and why abnormal insulin signaling culminates in synaptic failure and memory decline. We also discuss the cellular basis underlying the beneficial effects of stimulation of brain insulin signaling on cognition. Discoveries summarized here provide pathophysiological background for identification of novel molecular targets and for development of alternative therapeutic approaches in AD


-------------------------------------
Blocking Inflammation From PUFA Reverses Brain Aging

JNK And Tumor Necrosis Factor-alpha Mediate Free Fatty Acid-induced Insulin Resistance In 3T3-L1 Adi

"type 3 diabetes" - PubMed - NCBI
 

Peater Piper

Member
Joined
Mar 18, 2016
Messages
751
There's been some research in bypassing the problem with ketones, either through diet or using large amounts of MCTs. Correcting the insulin resistance would be ideal, though.
 

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