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Alzheimer's disease linked to abnormal cell division

A study in mice suggests that Alzheimer's disease may be triggered when adult neurons try to divide.

The study is published in in The Journal of Neuroscience.

For unknown reasons, neurons affected by Alzheimer's disease and many other neurodegenerative diseases often start to divide before they die.
The new study shows that, in animal models of Alzheimer's disease, this abnormal cell division starts long before amyloid plaques or other markers of the disease appear.
Cell division occurs through a process called the cell cycle.

" If you could stop cell cycling, you might be able to stop neurons from dying prematurely. This could be a fresh approach to therapy for Alzheimer's and other diseases, including stroke, amyotrophic lateral sclerosis, and HIV dementia, " says Karl Herrup, of Case Western Reserve University in Cleveland, who led the study.

The researchers compared the brains of three different mouse models of Alzheimer's disease to brains from normal mice, looking specifically for markers of cell cycling.
They found that, in the Alzheimer's disease mouse models, cell cycle-related proteins appeared in neurons 6 months before the first amyloid plaques or disease-related immune reactions developed in the brain.

Many of the neurons also had increased numbers of chromosomes, which is typical of cells that have begun to divide. These changes were not seen in normal mice.

The regions of the brain most affected by the neuronal cell cycling were the cortex and the hippocampus – the same regions most affected in Alzheimer's disease.
The cortex is important for thought and reasoning, while the hippocampus plays a key role in learning and memory.
Some parts of the brainstem also showed evidence of cell cycling.

While the cell cycling appeared to be necessary for neurons to die, it was not an immediate cause of cell death in the mouse models of Alzheimer's disease.
Instead, the affected neurons appeared to live for many months in a near-functional state, with the mice showing only mild behavioral changes during that time.
This suggests that another type of cellular problem, still unidentified, must damage the neurons in order for them to die.

The findings shed new light on the theory that the accumulation of amyloid beta in the brain causes the neuron death in Alzheimer's disease.
Because the abnormal cell cycling begins months before the formation of amyloid plaques, it is unlikely that the plaques themselves trigger the disease process.
However, tiny clumps made up of several amyloid beta molecules ( called micro-molecular aggregates ) form before the plaques and may trigger the disease. Since the three mouse models tested in this study all had mutations in the gene that codes for amyloid precursor protein, the similarity between affected brain regions in these mice and in people with Alzheimer's disease also supports the amyloid hypothesis.

While previous studies have linked Alzheimer's disease to abnormal cell cycling, this is the first study to examine the link using standard mouse models of Alzheimer's disease.

The results indicate that the mice, which do not develop neurofibrillary tangles or the severe behavioral symptoms of Alzheimer's disease, are accurate models of the early cellular processes that lead to the disease.

" The cell cycle markers mimic the human situation rather well," says Herrup. " This opens a range of new experimental possibilities using the cell cycle events as indicators of neuronal distress."

Herrup and his colleagues are now trying to determine if feeding the mouse models the drug Ibuprofen can stop abnormal cell cycling in neurons and halt neurodegeneration.
Ibuprofen is an anti-inflammatory drug that reduces production of amyloid beta, and some studies have suggested that it may reduce the risk of Alzheimer's disease.

The researchers are also planning additional studies to identify why neurons start to divide when they are diseased and why entering the cell cycle appears to trigger cell death.

Source: National Institutes of Health, 2006