Institute Activities

Speaker: Uri Alon

Title: Mathematical Essence of Aging

Date: TBD

Place: TBD

Fragile bones, deteriorating posture, and frequent fractures are all well-known hallmarks of old age. In a pair of recent studies, one published in Cell Reports and the other one in Developmental Cell, Prof. Elazar Zelzer and his team in the Department of Molecular Genetics examined the role of a sensory feedback system in muscles that guides both healing fractures and maintains the alignment of the spine.

Each group of long skeletal muscles contains sensory fibers that detect changes in the length of the muscle and report this information to the brain.  Called the proprioceptive system, this feedback loop between muscles and the brain plays a key role in guiding the growth and repair of bones, and in maintaining posture. Prof. Zelzer and his group have been studying the repair of fractures for a long time. They noticed that newborn mice had the ability to repair leg fractures naturally. These unstabilized fractures in the humerus were able to undergo spontaneous realignment, which they termed “natural reduction.”

Detecting the genes for hereditary neurodegeneration is challenging. In the case of ALS (Amyotrophic lateral sclerosis), commonly known as Lou Gehrig's disease, the disease-associated genes that have been identified explain only a small part of the cases. Prof. Eran Hornstein of the Department of Molecular Genetics studies microRNAs, suggesting they influence motor neuron development and survival.

MicroRNAs (abbreviated miRNA) are non-coding RNA molecules that play key roles in the process of gene expression. They are major regulators in a wide spectrum of neuronal processes and are pointed out as involved in diseases such as Alzheimer’s, Parkinson’s, and Huntington’s and also conditions involving motor neurodegeneration.

Cognitive decline in Alzheimer’s disease (AD) is associated with a range of physical changes in the brain: a loss of both brain cells and their interconnection points, and the accumulation of tangled neural fibers and plaques of misfolded amyloid-β protein. Most AD therapeutics use immunological and pharmacological tools to target the proteins thought to be responsible for these pathological changes, with mixed results. In addition, treating brain inflammation, which often accompanies neurodegenerative diseases, with nonsteroidal anti-inflammatory drugs has proven ineffective in halting disease progression.

In this review article Prof. Michal Schwartz in the Department of Neurobiology weighs the evidence and suggests revisiting therapeutic options. She recommends shifting focus to the role of the immune system in neurodegenerative diseases such as AD. In particular, she argues that methods for recruiting the brain’s own immune cells, called microglia, to target and destroy tangles and plaques, may be the key to combatting AD.