Murray A M, Weihmueller F B, Marshall J F, Hurtig H I, Gottleib G L, Joyce J N
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia 19104-6141.
Ann Neurol. 1995 Mar;37(3):300-12. doi: 10.1002/ana.410370306.
Parkinsonism occurs in approximately 35 to 40% of patients with Alzheimer's disease (AD) even with little or no neuronal degeneration in the substantia nigra, which in idiopathic Parkinson's disease (PD) results in the severe loss of striatal dopamine transporter sites. It is not known if there is a loss of striatal dopamine transporter sites in AD with coexistent parkinsonism (AD/parkinsonism). We quantified the pattern of these sites in the striatum and midbrain of patients with the clinical diagnosis of PD, AD, and AD/parkinsonism in comparison with a group of age-matched control subjects. We also quantified the number of D2 receptors and the levels of tyrosine hydroxylase in the substantia nigra and ventral tegmental area of the same groups. The results showed that in AD the loss of dopamine transporter sites was restricted to the nucleus accumbens. The loss of these sites in the AD/parkinsonism group was more extensive than in the AD group, with the most severe losses in the rostral caudate and putamen and least in the caudal caudate and putamen. While the PD group showed an equally severe reduction in numbers of sites, the caudal to rostral gradient of loss differed from that in the AD/parkinsonism group. The PD group also showed a marked loss of dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors (located on dopamine neurons) in the substantia nigra and ventral tegmental area. In contrast, no reductions in dopamine transporter sites, tyrosine hydroxylase, and D2 autoreceptors were observed in the substantia nigra and ventral tegmental area of the AD or AD/parkinsonism groups. Thus, the loss of striatal dopamine transporter sites in AD/parkinsonism may be related to the clinical parkinsonian symptoms. However, the loss is not simply the result of neuronal degeneration in the substantia nigra, but must derive from other processes.
帕金森综合征发生在约35%至40%的阿尔茨海默病（AD）患者中，即使黑质中几乎没有或没有神经元变性，而在特发性帕金森病（PD）中，这会导致纹状体多巴胺转运体位点的严重丧失。目前尚不清楚伴有帕金森综合征（AD/帕金森综合征）的AD患者是否存在纹状体多巴胺转运体位点的丧失。我们对临床诊断为PD、AD和AD/帕金森综合征的患者纹状体和中脑这些位点的模式进行了量化，并与一组年龄匹配的对照受试者进行了比较。我们还对同一组患者黑质和腹侧被盖区的D2受体数量和酪氨酸羟化酶水平进行了量化。结果显示，在AD中，多巴胺转运体位点的丧失仅限于伏隔核。AD/帕金森综合征组中这些位点的丧失比AD组更广泛，在尾状核头和壳核中丧失最严重，在尾状核尾和壳核中丧失最少。虽然PD组位点数量同样严重减少，但从尾端到前端的丧失梯度与AD/帕金森综合征组不同。PD组在黑质和腹侧被盖区还显示出多巴胺转运体位点、酪氨酸羟化酶和D2自身受体（位于多巴胺神经元上）的显著丧失。相比之下，在AD或AD/帕金森综合征组的黑质和腹侧被盖区未观察到多巴胺转运体位点、酪氨酸羟化酶和D2自身受体的减少。因此，AD/帕金森综合征中纹状体多巴胺转运体位点的丧失可能与临床帕金森症状有关。然而，这种丧失并非简单地是黑质神经元变性的结果，而必定源于其他过程。
