A new study reports that disease progression in Alzheimer’s disease (AD) gets worse when glucose transport across the blood brain barrier is impaired.
There are an estimated 72,000 people living with AD in Connecticut (5.2 million in the United States). There is no cure for AD. In one year alone (2010 data), Alzheimer’s was reported as the underlying cause of 820 deaths in Connecticut.
Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. This occurs because the first neurons to malfunction and die are usually neurons in brain regions involved in forming new memories. As neurons in other parts of the brain malfunction and die, the ability to carry out even the simplest tasks is destroyed.
Alzheimer’s disease was first identified more than 100 years ago, but research into its symptoms, causes, risk factors, and treatment has only gained momentum in the last 30 years. Although research has revealed a great deal, little is understood about the precise biologic changes that cause AD, why it progresses at different rates among affected individuals, and how the disease can be prevented, slowed, or stopped.
Glucose in circulating blood provides the primary energy source to the brain. AD is characterized by early reductions in glucose transport into the brain. This reduction in glucose transport is associated with the glucose transporter, GLUT1. However, little is understood regarding how GLUT1 influences the progression of AD.
This recent study examined an animal model of AD in which glucose transport is disrupted. The reduction in GLUT1 in this animal model caused an increase in neurodegeneration, blood vessel breakdown, and behavioral impairments. The results suggest that GLUT1 reductions at the blood brain barrier occur before neurodegeneration and cognitive impairment in AD.
This study suggests that GLUT1 may be a potential therapeutic target to decrease the cell death and vascular damages associated with Alzheimer’s. More research is needed to determine the molecular mechanisms behind GLUT1 reduction.
