Abstract
The clinical diagnosis of Alzheimer’s disease (AD) depends upon a history of progressive cognitive impairments, lack of focal neurological signs, and laboratory tests that exclude other known causes of dementia (1,2). A definitive diagnosis of AD depends upon characteristic histopathological features, including abundant senile plaques and neurofibrillary tangles in the cortical neuropil (3,4). Other anatomical features include decreased numbers of neurons in the nucleus basalis of Meynert (5), the brain stem nucleus locus coeruleus (6,7), and the frontal and temporal cortices (8). Frequent neurochemical correlates of AD are decreased choline acetyltransferase (CAT), acetylcholinesterase (AChE), glutamic acid decarboxylase (GAD), and butyrylcholinesterase (BuChE) activities, and decreased somatostatin, norepinephrine, and serotonin levels (9–20). Diagnosis of AD would be enhanced greatly if it were possible to detect any of these pathological or neurochemical changes in patients before death. Without such measures, the clinical diagnosis of AD is confirmed pathologically in only 60–75% of the cases (21, 22); in these instances, Parkinson’s disease (PD) and vascular disease are the most prevalent unrecognized causes of dementia. This chapter describes our experience with two approaches that may render diagnosis of the dementias more accurate: morphological studies with magnetic resonance imaging (MRI) of the brain and biochemical analyses of neurotransmitter markers in the cerebrospinal fluid (CSF).
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Growdon, J.H. et al. (1986). Diagnostic Methods in Alzheimer’s Disease: Magnetic Resonance Brain Imaging and CSF Neurotransmitter Markers. In: Fisher, A., Hanin, I., Lachman, C. (eds) Alzheimer’s and Parkinson’s Disease. Advances in Behavioral Biology, vol 29. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2179-8_25
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