| Popis: |
Alzheimer’s disease (AD), a progressive cerebral neurodegenerative disorder with no effective treatment as yet, is known to affect 5–7% of the population over age 65. This disorder is characterized by a progressive deterioration of cognitive and mnemonic abilities. Morphological, neurochemical and behavioral studies indicate a major degeneration of the central cholinergic.system in AD (1, 2). There is also evidence that noradrenergic, serotonergic, and somatostatin-like immunoreactivity are abnormal in AD, though to a lesser extent (for reviews see refs. 3 and 4). The contribution of the cholinergic dysfunction to the cognitive symptoms in AD is indicated by a direct correlation between loss of presynaptic cholinergic markers and mental test scores (1, 2). Postmortem evaluations of brains from patients with AD have revealed a select degeneration of cholinergic cells in the basal forebrain which project to the cerebral cortex and hippocampus (reviews 1–3). This degeneration is associated with a marked reduction of presynaptic cholinergic indices in these brain regions involved in cognitive processes (5). Somewhat conflicting results were reported regarding muscarinic receptors in AD. A loss of M2 muscarinic receptors was reported in a few studies (6–8 but see also 9, 10) while postsynaptic muscarinic receptors are relatively unchanged (6–9), decreased (10) or even upregulated (11). |
