Parkinson’s-Alzheimer's 'Combo' Boosts Dementia

Neurodegenerative disorders such as Alzheimer's and Parkinson’s are bad enough on their own, taking a huge toll on a patient's mental abilities. But researchers at the University of California in Irvine (UCI) have recently determined that their combined actions are even worst. The team says that the combinations of proteins that underlie the two distinct conditions contribute significantly to an acceleration of mental and cognition decline in affected individuals. The degradation occurs a lot faster than if only one of these two conditions had affected that patient.

The “combo” these two diseases create is called the Lewy body variant of Alzheimer’s, and this basically means that patients also exhibit signs of Parkinson’s. The condition is triggered by an interplay of proteins underlying the distinct disorders, which combine to create a potent inhibitor of various cognitive abilities. Slow regression of mental and physical capabilities is also a common side-effect in these two conditions, but only when taken separately. The regression is considerably boosted when the Lewy body disease sets in.

The molecular interactions between various classes of proteins in these instances were the object of a new study carried out by scientists at the UCI Institute for Memory Impairments and Neurological Disorders (MIND). The group was led by the Chancellor’s Professor of neurobiology & behavior Frank LaFerla, who is also the UCI MIND director. The team says that it engaged in this research because of the large number of people suffering from the Lewy body variant – half of all Alzheimer's patients, and about 1.3 million people in the United States alone.

The UCI team produced an animal model, designed specifically to replicate the effect of Lewy bodies in mice. Researchers knew that beta-amyloid protein plaques and tau protein tangles were a trademark of Alzheimer's, while alpha-synuclein protein accumulations were a hallmark of Parkinson’s. The mouse model exhibited all of these proteins. “Mouse models such as this are opening a window to the complex biological activity that underpins neurodegenerative diseases like Alzheimer’s and Parkinson’s. With enhanced research methods, we’re increasing our abilities to discover treatments,” LaFerla explains.

“We found the combination of these proteins in the same mouse accelerated the onset of the diseases. The proteins appeared to exacerbate ‘clumping up',” explains Mathew Blurton-Jones, who is an UCI assistant researcher in neurobiology and behavior. Details of the new work were published in the May 26 issue of the esteemed Journal of Neuroscience.