In contrast, among proteins showing a steep reduction in abundance in AD, a number were involved in SMC function (ACTA2, TAGLN, TPM1, TPM2, PGM5) and extracellular matrix (DES, OGN, CPXM1, PAPPA, FMOD) which may suggest cell loss or subtype shifting in response to amyloid deposition in brain parenchyma and cerebral blood vessels (Figure 4A). This evidence concerns the gene FMOD and Alzheimer disease.