A study from King’s College London’s Institute of Psychiatry, Psychology & Neuroscience reveals insights into how Alzheimer’s disease impacts pain perception, offering potential for enhanced patient care. The research delves into the enigmatic realm of pain in Alzheimer’s, challenging conventional beliefs about altered pain experiences in affected individuals.
Chronic musculoskeletal pain remains untreated in Alzheimers patients
Individuals with Alzheimer’s often experience untreated chronic musculoskeletal pain due to the challenges in communication caused by cognitive deficits. The recent study revealed a crucial pathway facilitating communication between sensory neurons and microglia in the spinal cord during inflammatory arthritis pain.
Microglia play an active role in influencing the body’s response to pain by responding to specific molecular cues. Research underscores the pain-enhancing effects of the protein Galectin-3 (Gal-3) under normal conditions. In a healthy body, pain signals travel to the central nervous system, initiating an immune response. Gal-3 facilitates the transmission of pain signals to the spinal cord, where they bind to another protein, TLR4, triggering the immune response.
In situations where the TLR4 protein is eliminated, the aforementioned impact is not observed, highlighting the significance of this protein in the processing of pain.
Researchers employed a mouse model replicating rheumatoid arthritis to investigate the topic. By inducing the chronic inflammatory disease in some mice through blood transfer, they noted variations in pain signal processing compared to healthy mice. The induced inflammation led to an increase in allodynia, a pain response triggered by a usually non-painful stimulus. Furthermore, heightened activation of microglia was observed, and these effects were identified as being controlled by TLR4.
TLR4 controls processing of pain signals
Researchers discovered that mice without TLR4 in their central nervous system’s immune cells exhibited a distinct pain response. These mice experienced reduced pain related to joint inflammation and a diminished immune response.
The study reveals that Gal-3, released by nociceptive neurons in the spinal cord, triggers microglia to adopt a TLR4-dependent profile, crucial for processing pain signals. This dynamic response to increased nervous system activity suggests implications for altered pain processing in Alzheimer’s patients, emphasizing the importance of TLR4.