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UK research paves the way for Alzheimer’s treatment

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Researchers in the UK have identified a potential target for drugs to treat long-term neurological conditions like Alzheimer’s Disease and foster nerve regeneration in central nervous system (CNS) injuries. 

The University of Birmingham research is part of a workstream exploring the signalling pathways behind ‘programmed cell death’.

This occurs in both long-term neurological conditions and spinal cord or optic nerve injuries.

Nerve cells are unable to fully repair this damage, resulting in the activation of the cell’s DNA damage response (DDR) system.

The persistent activation of this system affects CNS function and can trigger programmed cell death called apoptosis.

Professor Ahmed of the University of Birmingham’s Institute of Inflammation and Ageing explained:

“Our research started out exploring DNA damage pathways activated following nerve injury.

“However, the same molecular factors feature in pathways are seen in neurodegenerative diseases, and a full understanding of these mechanisms is an important step towards identifying potential targets for drug treatments.”

The research paper, which is published today, follows two recently published studies in spinal cord injury from the same research group.

The first study showed that an existing drug may reduce damage after spinal cord injury, by blocking the inflammatory response in the spinal cord.

The second study demonstrated that a brain-penetrating candidate drug currently in development as a cancer therapy can foster nerve repair after injury.

The current study focused on pathways that include enzymes called Checkpoint kinase 1 (Chk-1) and Checkpoint kinase 2 (Chk-2).

These act as gatekeepers to the DDR system, and can be inhibited using small molecules called Checkpoint kinase inhibitors (Chk-is).

The researchers first looked at a fruit fly model of amyloid toxicity, which occurs in neurological diseases when abnormal levels of this naturally occurring protein cluster together, disrupting nerve cell function.

The researchers learned that reducing Chk1 or Chk2 expression had a protective effect.

They then looked to animal neurotrauma models of optic nerve damage and spinal cord injury.

In optic nerve damage which occurs in patients with Alzheimer’s, MS, Parkinson’d disease and glaucoma,  the animal models showed administration of Chk-2is promoted nerve cell survival, and resulted in significant nerve regeneration with improved function of the optic nerve after injury.

These results were mirrored in spinal cord injury, where administration into the spinal canal promoted significant regrowth of nerve cells beyond the site of the injury, leading to a full restoration of the previously impaired sensation and movement after three weeks.

Professor Ahmed commented:

“These findings are truly exciting.

“They support a growing body of evidence that Chk-2 kinase inhibition can be both neuroprotective, and neuroregenerative, and provides a potential target for drug treatments for neurological diseases such as Alzheimer’s disease, Parkinson’s disease and Amyotrophic Lateral Sclerosis.”

Dr Richard Tuxworth from the Institute of Cancer and Genomic Sciences, added:

“This study raises the possibility of a completely new treatment strategy for a variety of neurodegenerative diseases, that is aimed at supporting nervous system function and slowing the progression of disease.”

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