It has been accepted by most scientists studying Alzheimer’s disease that the cause of the disease is the buildup of beta amyloid plaque in the brain. This buildup interferes with the normal functioning of the brain’s synapses. Synapses constitute the connections between brain cells. Those synapses form the network which allows information to be shared with different parts of the brain. Therefore, damage to the synapses leads to impaired mental function.
Recently, however, researchers at the Gladstone Institutes in San Francisco, CA, identified a second mechanism that diminishes proper functioning of the brain’s synapses. The team’s research demonstrated that this secondary mechanism is an important contributing factor to Alzheimer’s disease. Their findings were published in the journal Neuron.
The researchers, led by Dr. Katerina Akassoglou, began by analyzing problems in the network of blood vessels that appear in the brains of individuals with dementia. Their analysis led to the discovery of a specific protein, known as fibrinogen, that leaks into the brain and disrupts the synapse network.
Using advanced imaging technology to scan the brains of people with Alzheimer’s disease, as well as mice designed to have a form Alzheimer’s, the researchers found that fibrinogen leakage triggers an immune response, which leads to the destruction of synapses.
Confirmation of the team’s findings was accomplished by blocking the ability of fibrinogen to cause an immune response in the brains of the Alzheimer’s mice. Blocking the immune response protected the mice from the memory loss associated with Alzheimer’s disease.
In the words of Dr. Akassglou, “We found that blood leaks in the brain can cause elimination of neuronal connections that are important for memory functions. This could change the way we think about the cause and possible cure of cognitive decline in Alzheimer’s disease and other neurological diseases.”
The researchers demonstrated that even when no buildup of beta-amyloid plaque was present, fibrinogen leakage led to the destruction of synapses. And individuals who have both of these conditions experience faster rates of cognitive decline.
Most current therapies target the buildup of beta-amyloid plaque. This new research opens new avenues for therapies that can protect the brain against fibrinogen leakage, and, thus, against Alzheimer’s.
The best possible treatment for Alzheimer’s may lie in the future, but the best care for people with Alzheimer’s is available right now. At Hamilton Grove Healthcare and Rehabilitation Center, in Hamilton, NJ, we are experts in handling all levels of cognitive impairment, from mild cognitive impairment to Alzheimer’s and other dementias.
We have created a unique environment care program specifically designed to address the needs of this population. Our Alzheimer’s Unit is situated in a separate, secure wing to ensure the safety and well-being of our residents. It offers a structured daily routine, mind-stimulating activities, excellent social interaction, with optimal patient independence in a calm and soothing atmosphere.
Or better yet, come see for yourself: Contact us to schedule a tour by calling 609-588-5800 or by clicking here.