More evidence that Alzheimer’s is inflammatory

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“…Alzheimer’s and Parkinson’s are partly attributable to brain inflammation…”

Potential Alzheimer’s treatment? Newly discovered role for enzyme in neurodegenerative diseases

March 11, 2011
Karolinska Institutet
Neurodegenerative diseases like Alzheimer’s and Parkinson’s are partly attributable to brain inflammation. Researchers at Karolinska Institutet now demonstrate in a paper published in Nature that a well-known family of enzymes can prevent the inflammation and thus constitute a potential target for drugs.

Research suggests that microglial cells — the nerve system’s primary immune cells — play a critical part in neurodegenerative diseases, such as Alzheimer’s and Parkinson’s. The over-activation of these cells in the brain can cause inflammation, resulting in neuronal death.

Scientists at Karolinska Institutet and Seville University, working in collaboration with colleagues at Lund University, have now found a way to prevent the activation of the microglia and consequently the inflammation they cause. The key is the blocking of enzymes called caspases, which the team has shown control microglial activation.

“The caspases are a group of enzymes known for causing cell death,” says Associate Professor Bertrand Joseph, who headed the study. “That they also serve as signal molecules that govern that activity of other cells was an unexpected discovery that gives them an entirely new physiological role.”

By studying cell cultures and mice, the researchers show that certain caspases (3, 7 and 8) activate rather than kill microglial cells, which triggers an inflammatory reaction. Mice given caspase inhibitors displayed fewer activated microglia and less inflammation and cell death in the surrounding neurons.

They also examined samples from deceased Alzheimer’s and Parkinson’s patients and discovered a higher incidence of activated caspases in their microglial cells.

“We’ll now be examining whether the substances that inhibit the caspases can be candidates for useful drugs in the treatment of certain neurological diseases,” says Dr Joseph.

Journal Reference:

  1. Miguel A. Burguillos, Tomas Deierborg, Edel Kavanagh, Annette Persson, Nabil Hajji, Albert Garcia-Quintanilla, Josefina Cano, Patrik Brundin, Elisabet Englund, Jose L. Venero, Bertrand Joseph. Caspase signalling controls microglia activation and neurotoxicityNature, 2011; DOI: 10.1038/nature09788

Cancer drugs block dementia-linked brain inflammation, study finds

April 16, 2014
University of California – Irvine
A class of drugs developed to treat immune-related conditions and cancer — including one currently in clinical trials for glioblastoma and other tumors — eliminates neural inflammation associated with dementia-linked diseases and brain injuries, according to researchers. In their study, the researchers discovered that the drugs, which can be delivered orally, eradicated microglia, the primary immune cells of the brain. These cells exacerbate many neural diseases, including Alzheimer’s and Parkinson’s, as well as brain injury.

In their study, assistant professor of neurobiology & behavior Kim Green and colleagues discovered that the drugs, which can be delivered orally, eradicated microglia, the primary immune cells of the brain. These cells exacerbate many neural diseases, including Alzheimer’s and Parkinson’s, as well as brain injury.

“Because microglia are implicated in most brain disorders, we feel we’ve found a novel and broadly applicable therapeutic approach,” Green said. “This study presents a new way to not just modulate inflammation in the brain but eliminate it completely, making this a breakthrough option for a range of neuroinflammatory diseases.”

The researchers focused on the impact of a class of drugs called CSF1R inhibitors on microglial function. In mouse models, they learned that inhibition led to the removal of virtually all microglia from the adult central nervous system with no ill effects or deficits in behavior or cognition. Because these cells contribute to most brain diseases — and can harm or kill neurons — the ability to eradicate them is a powerful advance in the treatment of neuroinflammation-linked disorders.

Green said his group tested several selective CSF1R inhibitors that are under investigation as cancer treatments and immune system modulators. Of these compounds, they found the most effective to be a drug called PLX3397, created by Plexxikon Inc., a Berkeley, Calif.-based biotechnology company and member of the Daiichi Sankyo Group. PLX3397 is currently being evaluated in phase one and two clinical trials for multiple cancers, including glioblastoma, melanoma, breast cancer and leukemia.

Crucially, microglial elimination lasted only as long as treatment continued. Withdrawal of inhibitors produced a rapid repopulation of cells that then grew into new microglia, said Green, who’s a member of UC Irvine’s Institute for Memory Impairments and Neurological Disorders.

This means that eradication of these immune cells is fully reversible, allowing researchers to bring microglia back when desired. Green added that this work is the first to describe a new progenitor/potential stem cell in the central nervous system outside of neurogenesis, a discovery that points to novel opportunities for manipulating microglial populations during disease.

Study results appear in today’s issue of Neuron.

Journal Reference:
  1. Monica R.P. Elmore, Allison R. Najafi, Maya A. Koike, Nabil N. Dagher, Elizabeth E. Spangenberg, Rachel A. Rice, Masashi Kitazawa, Bernice Matusow, Hoa Nguyen, Brian L. West, Kim N. Green. Colony-Stimulating Factor 1 Receptor Signaling Is Necessary for Microglia Viability, Unmasking a Microglia Progenitor Cell in the Adult BrainNeuron, 2014; 82 (2): 380 DOI: 10.1016/j.neuron.2014.02.040

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