Characterized primarily by acute memory loss and rapidly degenerative cognitive abilities, Alzheimer’s disease continues to remain highly prevalent amongst the geriatric populace, across the globe, contributing amply towards the compromised quality of life. Nonetheless, the potential triggers and underlying causes of this degenerative condition is deficient in optimum research.
Ongoing endeavors are targeting to unleash path-breaking findings concerning disease prognosis and vital therapeutics.
According to new studies, Alzheimer’s disease amounts to the abnormal generation of protein plaques such as beta-amyloid in the brain which interfere with normal synapses functioning that contribute amply towards uninterrupted dissemination of information within the brain.
However, advances in Alzheimer’s disease therapeutics aimed at defining disease pathology and its probable treatment procedures have unveiled new milestones. In a recent development, veteran scientists at Gladstone Institute have affirmed the role of fibrinogen which essentially is a clotting protein in instrumenting cognitive degeneration by inhibiting regular functioning of neurons.
Fibrin Permeability in the Brain Renders Rapid Disease Occurrence
Although under normal conditions, fibrin remains highly non-permeable. However, in certain cases, permeability is lost, leading to instances of Alzheimer’s disease. The above conclusions have been verified by rigorous studies as well as ample animal testing. Illustrative research studies published in the journal Neuron, conclude that fibrinogen leakage into the brain triggers a rapid decline of synapses, thereby amounting to an inefficient communication matrix within the brain.
With notable advances in preventive medication, scientists opine the prevalence of certain genes such as Apo-E4 elevates chances of Alzheimer’s in later years, multiplying disease vulnerability. The gene commonly inherited in pairs from biological parents. Prevalence of at least one such APOE4 gene naturally contributes towards disease occurrence. Based on such preliminary studies, ample research initiatives directed towards altering gene functionality to arrest instances of Alzheimer’s disease.