A high ratio of chromogranin A to synaptin/synaptophysin is a common feature of brains in Alzheimer and Pick disease

Abstract

Chromogranin A and synaptin/synaptophysin were characterized by immunological methods in human autopsy brain tissue from patients with Alzheimer's and Pick's disease. In immunoblots there was no qualitative difference between the antigens in control and diseased brain, but significant quantitative differences were found. In all Alzheimer cases there was a significantly lower level of synaptin/synaptophysin, whereas chromogranin A was higher in 4 out of 5 cases and in all cases relative to synaptin/synaptophysin. An analogous findingwas obtained for Pick's disease. Immunohistologically a consistent staining of neuritic plaques for chromogranin A, but not for secretogranin II was found in Alzheimer cases. In Pick's disease the characteristic Pick bodies showed an analogous specific immunostaining.

Cloning and Expression of a Brain-Specific Putative UDP-GalNAc: Polypeptide N-Acetylgalactosaminyltransferase Gene

“…31,33) CgA is also reported to accumulate in patients with Parkinson's disease and Pick's disease. [34][35][36] O-Glycosylation of a-synuclein is reported as well.…”

Stereologic estimates of total spinophilin-immunoreactive spine number in area 9 and the CA1 field: Relationship with the progression of Alzheimer's disease

“…Several studies have shown that in addition to these traditionally described lesions, AD is characterized by selective neuronal loss [30,72], severe and early loss of synapses [15,16,24,45,59], and synaptic pathology [41,44]. Early immunocytochemical studies indicated an average 45% decrease in presynaptic terminal density in the AD neocortex [44,45,76]. Quantitative morphometric study of temporal and frontal cortical biopsies performed within an average of 2 to 4 years from the onset of clinical AD revealed 25 to 35% decrease in the numerical density of synapses and 15 to 35% decrease in the number of synapses per cortical neuron [15].…”

Chromogranin A in Cerebrospinal Fluid: A Biochemical Marker for Synaptic Degeneration in Alzheimer’s Disease?

“…CrA is present in the brain, where the concentration is highest in the neocortex [11], while it is not found in the white matter [12,13]. Immunohistochemically, CrA is found in a granular distribu tion in the neuronal perikarya, dendrites, and synapses [12][13][14], a distribution consistent with a location in the large dense-core synaptic vesicles, which has been con firmed ultrastructurally [15][16][17],…”

“…In addition, CrA is found in senile plaques [18,19], especially in such with a neuritic component [13,14], although also present in diffuse (3A4 amyloid deposits (diffuse plaques) [20], and in a recently described type of lesion, tangle-associated neuritic clusters, composed of aggregates of abnormal neurites centred by an extracellu lar NFTs [ 19],…”