Scientists have long debated whether Alzheimer’s disease starts in separate regions of the brain independently and at different times, or if it begins in one region and then spreads. Data from researchers at Columbia University Medical Center supports the latter model, showing that abnormal tau protein — a key feature observed in the brains of patients with Alzheimer’s disease — propagates along anatomically connected networks, between connected and vulnerable neurons. The study was published earlier this month in the online journal PLoS ONE [1].

Image credit: Neurons network in human brain via Shutterstock

Key cells in the brain region known as the hippocampus are formed in the base of the brain late in fetal life and undertake a long journey before reaching their final destination in the center of the brain shortly after birth, according to researchers at the National Institutes of Health (NIH).

Memories are fragile; initially forming and then retrieving them are both dependent on new protein synthesis in the brain, and both processes are vulnerable to disruption. A number of agents are known that can impair memory and these can certainly be useful — for example, in treating post-traumatic stress disorder (ptsd). Enhancing memory, however, has proven more difficult. Yet as noted in The New York Times last week [1], two different research groups have recently reported enhancing memory in rats [2-3]. Of note is the fact that they did so utilizing independent molecular pathways.

A naturally occurring growth factor significantly boosted retention and prevented forgetting of a fear memory when injected into rats’ memory circuitry during time-limited windows when memories become fragile and changeable. In a study funded by the National Institutes of Health (NIH), animals treated with insulin-like growth factor (IGF2) excelled at remembering to avoid a location where they had previously experienced a mild shock [1].