Maurizi C P
Med Hypotheses. 1987 Sep;24(1):59-68. doi: 10.1016/0306-9877(87)90047-8.
Anatomic, chemical, physiologic, pathologic and clinical evidence suggests that senile dementia (Alzheimer's disease) is a dysfunction of the hippocampus. Failure of hippocampal plasticity could be secondary to loss of input from the medial septal nucleus and/or locus ceruleus or due to a functional abnormality. When compared to age-matched controls, demented patients have decreased hippocampal norepinephrine and serotonin, increased hippocampal monoamine oxidase, and decreased REM sleep. These observations could be explained by a melatonin deficiency. A chronic melatonin deficiency, with loss of dreams, could cause dementia.
解剖学、化学、生理学、病理学及临床证据表明，老年痴呆症（阿尔茨海默病）是海马体功能障碍。海马体可塑性的丧失可能继发于内侧隔核和/或蓝斑核输入的丧失，或者是由于功能异常。与年龄匹配的对照组相比，痴呆患者海马体中的去甲肾上腺素和血清素减少，海马体单胺氧化酶增加，快速眼动睡眠减少。这些观察结果可以用褪黑素缺乏来解释。慢性褪黑素缺乏，伴随梦境丧失，可能导致痴呆。
