Carlesimo G A, Oscar-Berman M
Istituto di Neurologia, II Università di Roma, Italy.
Neuropsychol Rev. 1992 Jun;3(2):119-69. doi: 10.1007/BF01108841.
Despite considerable experimental work on Alzheimer's disease (AD), the underlying cognitive mechanisms as well as the precise localization of neuropathological changes critical for memory loss remains undefined. A review of the neuropsychological literature on long-term memory deficits in AD patients suggests that AD patients display (a) a pervasive deficit of explicit memory, (b) a partial deficiency of implicit memory for verbal and visuoperceptual material (as measured by repetition priming procedures), and (c) a substantial sparing of implicit memory for visuomotor skills. The explicit memory loss is likely a result of encoding as well as consolidation difficulties. A faulty lexical-semantic knowledge structure appears responsible for deficient repetition priming effects. Since neuropathological changes diffusely affect the brain of AD patients, establishing a clear relationship between localization of cerebral lesions and memory deficits is particularly difficult. Nevertheless, data suggest that extensive involvement of the hippocampal-amygdala complex plays a major role in explicit memory loss. Damage to associative cortical areas likely is involved in repetition priming deficits. The relative integrity of primary motor and sensory cortical areas and of the basal ganglia likely subsume, by contrast, the normal learning of visuomotor skills.
尽管针对阿尔茨海默病(AD)开展了大量实验研究,但对于其潜在的认知机制以及导致记忆丧失的神经病理变化的确切定位仍不明确。对有关AD患者长期记忆缺陷的神经心理学文献进行综述后发现,AD患者表现出:(a)外显记忆普遍受损;(b)对言语和视觉感知材料的内隐记忆部分缺失(通过重复启动程序测量);(c)视觉运动技能的内隐记忆基本未受影响。外显记忆丧失可能是编码以及巩固困难所致。词汇语义知识结构存在缺陷似乎是重复启动效应不足的原因。由于神经病理变化会广泛影响AD患者的大脑,因此在脑损伤定位与记忆缺陷之间建立明确的关系尤为困难。然而,数据表明海马体 - 杏仁核复合体的广泛受累在显性记忆丧失中起主要作用。联合皮质区域受损可能与重复启动缺陷有关。相比之下,初级运动和感觉皮质区域以及基底神经节的相对完整性可能是视觉运动技能正常学习的基础。