Institute of Memory and Alzheimer's Disease (IM2A), Department of Neurology, Assistance Publique-Hôpitaux de Paris (AP-HP), Sorbonne University, Pitié-Salpêtrière Hospital, 75013, Paris, France.
FrontLab, Paris Brain Institute (Institut du Cerveau, ICM), AP-HP, Pitié-Salpêtrière Hospital, 75013, Paris, France.
Commun Biol. 2024 Oct 24;7(1):1384. doi: 10.1038/s42003-024-07076-7.
Alzheimer's disease (AD) encompasses a long continuum from a preclinical phase, characterized by neuropathological alterations albeit normal cognition, to a symptomatic phase, marked by its clinical manifestations. Yet, the neural mechanisms responsible for cognitive decline in AD patients remain poorly understood. Here, we posit that anosognosia, emerging from an error-monitoring failure due to early amyloid-β deposits in the posterior cingulate cortex, plays a causal role in the clinical progression of AD by preventing patients from being aware of their deficits and implementing strategies to cope with their difficulties, thus fostering a vicious circle of cognitive decline.
阿尔茨海默病(AD)包括一个从临床前期到有症状期的漫长连续体,临床前期的特征是尽管认知正常,但存在神经病理学改变,有症状期的特征是其临床表现。然而,AD 患者认知能力下降的神经机制仍知之甚少。在这里,我们假设,由于后扣带回皮质早期的淀粉样蛋白-β沉积导致错误监测失败而出现的否认症,通过阻止患者意识到自己的缺陷并实施应对困难的策略,从而在 AD 的临床进展中起着因果作用,从而形成认知能力下降的恶性循环。