New mechanism for Alzheimer's disease


Rebecca Pool

Monday, June 1, 2015 - 12:45
Image: Laser scanning microcsopy of mouse brain.
Norway-based researchers have uncovered a new mechanism for Alzheimer's disease, revealing stunning images of the brains of mice with the condition.
Alzheimer's patients develop deposits of amyloid peptides in the brain that disrupt neuronal networks, leading to memory loss, behavioural changes and eventual death.
Research from Professor Jens Pahnke and his team from Neuropathology at the University Hospital Oslo, reveals that insufficient removal of these amyloid peptide plaques triggers Alzheimer's disease, rather than overproduction as had been previously assumed.
Stunning laser scanning microscopy images reveal red amyloid plaques surrounded by green astrocytes, the characteristic star-shaped glial cells found in the brain and spinal cord.
As Pahnke points out: "Microglia attack the beta-amyloid and try to remove it, which in fact, doesn't work very well."
Professor Jens Pahnke with a slide of brain hemisphere, showing demyelinated white matter. [Beachten ]
To investigate the hypothesis that Alzheimer's disease follows plaque accumulation, Pahnke and colleagues developed a method to disrupt the function of the genes needed to excrete and digest these peptides.
Laser scanning microscopy of mouse brain: Red Alzheimer plaque surrounded by green astrocytes, labelled in green anti-GFAP. Image taken using a Zeiss LSM. [Pahnke]
The researchers showed that mice without these genes developed early signs of the disease, supporting the hypothesis that insufficient toxic metabolite removal can lead to sporadic Alzheimer's disease.
"We showed that the mice have a reduced probability to survive, show increased anxiety in new environments and have a reduced working memory performance," says Pahnke. "We [also] detected changes in the hippocampus and amygdala... [including] a reduced number of synapses."
"This presents a new model for early effects of amyloid-beta-related mild cognitive impairment that allows investigations without artificial over-expression of inherited Alzheimer's disease genes," he adds.
Research is published in Brain.
Learn more about Jens Pahnke's research here.
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