Kurt Lucin Explains How Alzheimer’s Disease Might Progress

On April 3, Kurt Lucin, assistant professor of biology, continued the Faculty Scholars Forum with a discussion on Alzheimer’s Disease (AD), a debilitating neurological disease that affects a growing number of elderly people.

A comparison of a normal healthy brain and a brain with Alzheimer’s disease (AD). Severe degeneration and neuron loss can be observed in the AD brain, which appears shriveled and smaller in size.

Lucin says AD is characterized by a progressive loss of cells in the brain and a concomitant decline in cognitive function.

Shown are astrocyte cells that have internalized (phagocytosed) 6μm latex beads. Arrows indicate the phagocytosed beads.

“These impairments are associated with the appearance of amyloid plaques and neurofibrillary tangles within the brain.”

Shown are two astrocyte cells, one of which has internalized (i.e., phagocytosed) 6μm latex beads. Both astrocyte cells fluoresce green and the beads fluoresce red.

Lucin said previous studies indicate that AD is accompanied by reduced levels of the protein beclin 1 within diseased regions of the brain. Beclin 1 is involved in numerous processes, including a cellular degradation process, called autophagy, and the trafficking of recognition molecules called receptors.

A microscopic view of a human Alzheimer’s disease brain. Shown in brown are amyloid beta plaques, which are characteristic of the disease and accumulate as the disease progresses.

“My research is interested in understanding the consequences of reduced beclin 1 on disease progression,” said Lucin. “We are particularly interested in understanding how reduced beclin 1 may affect the function of astrocytes. Astrocytes are the most numerous cell in the brain, provide neuronal support, and are capable of internalizing and degrading amyloid plaques via a process called phagocytosis.”

By Dwight Bachman