The primary pathological manifestation of AD, the aggregates of amyloid beta (aβ) and the amyloid precursor protein (APP), are influenced by dysregulated chondroitin sulfates and heparan sulfates, which are associated with a higher protein-aggregate burden, along with increased amounts of the matrisome components tenascin, integrin, laminin, and galectin [50]. This evidence concerns the gene TNC and Alzheimer disease.