Reduced somatostatin-like immunoreactivity in cerebral cortex from cases of Alzheimer disease and Alzheimer senile dementa

Abstract

Both Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) are progressive dementias characterized neuropathologically by the presence in the cerebral cortex of numerous neurofibrillary tangles and neuritic plaques¹. We use the abbreviation AD/SDAT to denote all such cases, irrespective of age of onset². Studies of neurotransmitter-related parameters in autopsied brain tissues from patients with AD/SDAT have, to date, been confined to five putative transmitter systems. Acetylcholine-releasing neurones seem to be most markedly and consistently affected, as judged by the extensive reductions in choline acetyltransferase (ChAT) and acetylcholinesterase activities that have been reported^3–5. Despite numerous studies, there is no consistent evidence for the involvement of neurones releasing dopamine, noradrenaline, serotonin, or γ-aminobutyric acid in AD/SDAT⁶, nor for loss of muscarinic cholinergic receptors⁷. Thus, the involvement of cholinergic neurones in AD/SDAT seems to be specific. However, the possible involvement of neurones using other chemicals as transmitters has yet to be explored. The recent recognition of the existence of so-called ‘peptidergic neurones’ in the mammalian brain (for review see ref. 8) and the availability of radioimmunoassay (RIA) techniques for studying these peptides, have led us to begin a systematic investigation of neuropeptides in autopsied brain tissue from cases of AD/SDAT, and from neurologically normal individuals. We report here results obtained with a RIA for somatostatin, showing that somatostatin-like immunoreactivity in the cerebral cortex is reduced in tissue from AD/SDAT patients.