Scientists have discovered brain early loss patterns in rats that appear likely to be predictive of the risk of Alzheimers disease in humans.

They also found that many genes involved in learning and memory were changed in an area of the brain that is impacted by the development of Alzheimers disease. The study published in the scientific journal eLife suggests that brain circuits evolved during adolescence to allow us to learn and regulate our social interactions.

The findings could help answer fundamental questions about human brain function suggesting new treatments for Alzheimers disease where genetic variations may have been passed across generations.

Mutations in two genes that encode so-called neurexin protein proteins and affect the activity of neurons in the hippocampus a brain region that plays a key role in memory and learning have been identified in rats. Neurexin and protein can bind with nerve cells called neurons and operate like electrical switches. This allows neurons to control the activity of various brain networks regulating excitability the production of new brain cells and clearing away brain-damaging proteins.

As part of ongoing studies at the National Institute of Neurological Disorders and Stroke (NINDS) in Louisville Kentucky and University of Exeter in the UK the first authors of the study say they will focus on the changes in the brains neurogenesis the brains ability to grow new connections and synapses and the support structures that are needed to keep neurons active.

Neurexin which carries the same function in humans was only discovered a few decades ago but scientists were aware of changes in the rat brain in response to current medication for brain epilepsy. This study could provide a new insight into the social and cognitive aspects of learning and memory in humans already at early stages of pathological disease explained senior author and neuroscientist Dr Neil Shettis of NINDS US.

For the study rats fed a normal diet were found to have wrinkles spreading over their foreheads and body known as subtle body length loss suggesting that brain circuits passed on throughout adolescence may also be disrupted during Alzheimers disease. Rats that were known to be genetically mentered (high-producing blood cells) for Alzheimers disease had a normal brain growth of around 4. 2 millimetres per day similar to humans who are under 5 millimetres.

However detection of subtle body structural changes without cognitive performance were induced in all rat groups by administering alpha-synuclein an organic compound present in brain tissues. This proved to be the root cause of the differences observed in the brain of rats who expressed high levels of mE as a marker for psychiatric disorders.

The scientists also found that when the control groups had high levels of mE with no cognitive performance physical structure changes of the brain had also been induced once again which suggested that the brain assemblies affected by Lewy B deficiency may also be relevant in cognitive processes.