Alzheimer's disease leads to memory deficits and progressive
hippocampal neuron degeneration. Memory loss and other cognitive symptoms of Alzheimer's disease are
attributed, in part, to the degeneration of acetylcholine-producing
Acetylcholinesterase inhibitors are a common treatment for
patients with Alzheimer's; however, in spite of their clinical benefits,
these non-selective medications are also associated with numerous
adverse effects. It has been hypothesized that more selective targeting
of acetylcholine signaling may reduce the side effects associated with
current Alzheimer's medications, but it's not known whether improving
selectivity could decrease the treatment's efficacy.
‘Treatment with the M1-selective medications reversed memory deficits and profoundly extended the lifespan of the diseased mice.’
In December 2016 issue of the JCI
work led by Andrew Tobin at the University of Leicester tested two
drugs that specifically target the M1 muscarinic acetylcholine receptor
in a mouse model of neurodegeneration and discovered that the treatments
had promising effects.
The mouse model showed many hallmarks of human
Alzheimer's disease. Treatment with the M1-selective
medications reversed memory deficits and profoundly extended the
lifespan of the diseased mice.
These findings support the concept that
more specific drugs can be effective in treating the cognitive symptoms
of neurodegenerative disease. Future work is needed to determine whether
these potential medications are effective in humans, and whether the
improved targeting actually leads to fewer side effects.