Scientists at the University of Florida have found that a changed version of Associate in Nursing immune cell supermolecule can be used as a treatment for Alzheimer’s malady.
In a mouse model of the malady, the researchers found that a soluble version of toll-like receptor 5 (TLR5) reduced the accumulation of the toxic β-amyloid that causes the degeneration and death of neurons.
The immune system plays a role in the progression of Alzheimer’s disease by reducing the accumulation of β-amyloid aggregates or by triggering inflammation that goes on to cause further neuronal damage.
One family of proteins present on the surface of immune cells – TLRs − responds to nerve cell damage by inducing an immune response.
Paramita Chakrabarty and colleagues from the University of Florida recently found that the extent of those TLRs is higher within the brains of individuals with Alzheimer’s malady, part because of Associate in Nursing hyperbolic level of brain immune cells known as glia.
This semiconductor diode them to raise whether or not soluble versions of TLRs taken from glia might cut back amyloid protein plaque formation.
They hypothesized that the soluble TLRs could serve as “decoys” that bind to β-amyloid and reduce its accumulation, while not triggering the system to induce inflammation.
In a mouse model of Alzheimer’s where human β-amyloid is produced in large amounts, the team found that one soluble TLR known as TLR5 prevented and even reversed amyloid protein plaque formation.
As reportable within the Journal of Experimental medication, the team found that soluble TLR5 did indeed bind to β-amyloid and increased its uptake by microglia.
TLR5 also limited β-amyloid’s ability to damage nerve cells.
By directly interacting with β-amyloid and attenuating β-amyloid levels in mice, the soluble TLR5 decoy receptor represents a novel and potentially safe class of immunomodulatory agents for Alzheimer’s disease.” – Dr. Todd Golde, Co-author
“The potential of soluble TLR5 in wetting immune activation and connected toxin pathways has to be any explored in multiple models of Alzheimer’s,” concludes Chakrabarty.