ApoE4 and the Insulin Receptor — It's a Trap!


Posted by Richard C on Aug 1, 2018 3:15:00 AM

You might be surprised to learn that diabetes, a metabolic disease, may be linked to the neurodegenerative condition Alzheimer’s disease (AD). Diabetes is driven by altered insulin signaling from either insufficient insulin production (Type 1) or altered insulin receptor (IR) signaling (Type 2). In a seemingly unrelated disease, the human e4 allele of APOE is the strongest genetic risk factor for AD.

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Topics: Alzheimer's Disease, Neurodegeneration, Metabolism, Journal Club

Missing Link: Why Do Insulin-producing Cells in Type 2 Diabetes Fail to Divide?


Posted by Neha G on Jan 17, 2018 3:00:00 AM

Type 2 diabetes is a growing epidemic, and is recognized as one of the most serious metabolic disease worldwide. A multifactorial disease, type 2 diabetes is a perfect example of metabolic miscommunication between different organs resulting in a pathological outcome. According to CDC in the United States, 29.1 million people in the United States have diabetes, and 8.1 million may be undiagnosed. The disease affects more than 1 in every 10 adults, and seniors aged 65 and above are most affected. What makes the disease morbid are the secondary complications associated with it; atherosclerosis and cardiomyopathy are the leading cause of death in people diagnosed with type 2 diabetes. The need for an effective treatment has become a global health priority.

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Topics: Metabolism, Cell Biology, Journal Club

Webinar | Advances in AMPK and Autophagy Signaling


Posted by Liana G on Dec 20, 2017 6:15:00 AM

Reuben Shaw, Ph.D

Professor, Molecular and Cell Biology Laboratory, Deputy Director, Salk Cancer Center, The Salk Institute for Biological Studies

AMPK, a highly conserved sensor of cellular energy status, is found in all eukaryotic cells and maintains metabolic homeostasis by reprogramming growth, metabolism, and autophagy in the face of cellular stresses.

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Topics: Metabolism, Cell Biology

Journal Club: TREM2 Opens a Rabbit Hole of Questions for Alzheimer’s Researchers


Posted by Richard C on Nov 8, 2017 3:00:00 AM

It's almost time for the 2017 Society for Neuroscience meeting. To get your neurons excited for the meeting, here's a journal club discussing a recent paper with interesting findings for Alzheimer's disease. 

The pathological hallmark of Alzheimer’s disease (AD) is the accumulation of amyloid β (Aβ) plaques and neurofibrillary tangles. Despite decades of research, the direct (and indirect) contribution of these lesions in disease progression is poorly understood. Do these lesions directly cause neuronal dysfunction and neurodegeneration? If so, why do some patients accumulate these lesions, but exhibit normal neurological behavioral before death? Do AD patients have secondary defects in cellular and/or molecular processes that normally function to protect patients from accumulation of these nefarious lesions? If so, what are these cell types and what…

Wait.

Take a breath.

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Topics: Journal Club, Neuroscience, Autophagy, Alzheimer's Disease, Neurodegeneration, Metabolism

Webinar - Advancements in AMPK and Autophagy Signaling


Posted by Liana G on Nov 18, 2015 3:30:00 AM

Reuben Shaw, Ph.D

Professor, Molecular and Cell Biology Laboratory, Deputy Director, Salk Cancer Center, The Salk Institute for Biological Studies

AMPK, a highly conserved sensor of cellular energy status, is found in all eukaryotic cells and maintains metabolic homeostasis by reprogramming growth, metabolism, and autophagy in the face of cellular stresses. AMPK is activated by direct binding of AMP and ADP to its regulatory subunits, which enhances its phosphorylation by the upstream kinase LKB1, a tumor suppressor gene frequently inactivated in sporadic human lung and cervical cancer.

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Topics: Metabolism, Cell Biology

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