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Arch Neurol. 2003;60:320.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

CLINICOPATHOLOGIC EXAMINATION of human brains is the traditional starting point for our understanding of disease pathophysiology, disease treatment, and the functional-anatomical organization of the brain. In this issue of the ARCHIVES, Zarow et al¹ report major cell loss in the brainstem, noradrenergic locus coeruleus (LC), in brains from patients with Alzheimer disease (AD) and Parkinson disease (PD) compared with healthy controls. The findings are, per se, not surprising as LC pathology has been previously documented in experimental and idiopathic parkinsonism.² What is remarkable is the observation that LC neuron loss is uniformly severe across PD cases and roughly 75% of AD cases. Moreover, the degree of LC loss appears more extensive than that in 2 brain regions to which the main clinical features of AD and PD are commonly ascribed: cholinergic neurons of the nucleus basalis (AD) and dopaminergic neurons in the substantia nigra (PD). While the analysis by Zarow . . . [Full Text of this Article]

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