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). The gene discussed is TAGLN; the disease is Alzheimer disease.