Cognitive Impairment in Idiopathic Normal Pressure Hydrocephalus.
10.1007/s12264-022-00873-2
- Author:
Haoyun XIAO
1
;
Fan HU
2
;
Jing DING
3
;
Zheng YE
4
Author Information
1. Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
2. Department of Neurosurgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
3. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
4. Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China. yez@ion.ac.cn.
- Publication Type:Review
- Keywords:
Amyloid-β pathology;
Cerebrospinal fluid dynamics;
Cognitive impairment;
Entorhinal-hippocampal circuits;
Frontostriatal circuits;
Idiopathic normal pressure hydrocephalus;
Neuromodulation;
Tau pathology
- MeSH:
Aged;
Cognitive Dysfunction/etiology*;
Humans;
Hydrocephalus, Normal Pressure/diagnosis*;
Peptide Fragments;
Quality of Life;
tau Proteins
- From:
Neuroscience Bulletin
2022;38(9):1085-1096
- CountryChina
- Language:English
-
Abstract:
Idiopathic normal pressure hydrocephalus (iNPH) is a significant cause of the severe cognitive decline in the elderly population. There is no cure for iNPH, but cognitive symptoms can be partially alleviated through cerebrospinal fluid (CSF) diversion. In the early stages of iNPH, cognitive deficits occur primarily in the executive functions and working memory supported by frontostriatal circuits. As the disease progresses, cognition declines continuously and globally, leading to poor quality of life and daily functioning. In this review, we present recent advances in understanding the neurobiological mechanisms of cognitive impairment in iNPH, focusing on (1) abnormal CSF dynamics, (2) dysfunction of frontostriatal and entorhinal-hippocampal circuits and the default mode network, (3) abnormal neuromodulation, and (4) the presence of amyloid-β and tau pathologies.
