Sea Cucumber-Derived Peptide Attenuates Scopolamine-Induced Cognitive Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

2022 ◽  
Author(s):  
Yue Zhao ◽  
Zhiqiang Lu ◽  
Xiaomeng Xu ◽  
Na Sun ◽  
Songyi Lin
Keyword(s):  
Cell Death ◽  
Cognitive Impairment ◽  
Sea Cucumber ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cholinergic Dysfunction

From tau phosphorylation to tau aggregation: what about neuronal death?

2010 ◽  
Vol 38 (4) ◽  
pp. 967-972 ◽  
Author(s):  
Luc Buée ◽  
Laëtitia Troquier ◽  
Sylvie Burnouf ◽  
Karim Belarbi ◽  
Anneke Van der Jeugd ◽  
...  
Keyword(s):  
Cell Death ◽  
Cognitive Impairment ◽  
Neurodegenerative Disorders ◽  
Neuronal Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Tau Phosphorylation ◽  
Tau Proteins ◽  
Phosphorylated Tau ◽  
Sequence Of Events

Tau pathology is characterized by intracellular aggregates of abnormally and hyperphosphorylated tau proteins. It is encountered in many neurodegenerative disorders, but also in aging. These neurodegenerative disorders are referred to as tauopathies. Comparative biochemistry of the tau aggregates shows that they differ in both tau isoform phosphorylation and content, which enables a molecular classification of tauopathies. In conditions of dementia, NFD (neurofibrillary degeneration) severity is correlated to cognitive impairment and is often considered as neuronal death. Using tau animal models, analysis of the kinetics of tau phosphorylation, aggregation and neuronal death in parallel to electrophysiological and behavioural parameters indicates a disconnection between cognition deficits and neuronal cell death. Tau phosphorylation and aggregation are early events followed by cognitive impairment. Neuronal death is not observed before the oldest ages. A sequence of events may be the formation of toxic phosphorylated tau species, their aggregation, the formation of neurofibrillary tangles (from pre-tangles to ghost tangles) and finally neuronal cell death. This sequence will last from 15 to 25 years and one can ask whether the aggregation of toxic phosphorylated tau species is a protection against cell death. Apoptosis takes 24 h, but NFD lasts for 24 years to finally kill the neuron or rather to protect it for more than 20 years. Altogether, these data suggest that NFD is a transient state before neuronal death and that therapeutic interventions are possible at that stage.

scholarly journals Disruption of Bax Protein Prevents Neuronal Cell Death but Produces Cognitive Impairment in Mice following Traumatic Brain Injury

2008 ◽  
Vol 25 (7) ◽  
pp. 755-767 ◽  
Author(s):  
Roya Tehranian ◽  
Marie E. Rose ◽  
Vincent Vagni ◽  
Alicia M. Pickrell ◽  
Raymond P. Griffith ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Death ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Bax Protein

scholarly journals Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models

2007 ◽  
Vol 32 (11) ◽  
pp. 2393-2404 ◽  
Author(s):  
Yoori Choi ◽  
Hye-Sun Kim ◽  
Ki Young Shin ◽  
Eun-Mee Kim ◽  
Minji Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Cognitive Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Disease Models

scholarly journals Is there a neuropathology difference between mild cognitive impairment and dementia?

2009 ◽  
Vol 11 (2) ◽  
pp. 171-179 ◽  
Keyword(s):  
Cell Death ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Function ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Normal Function ◽  
Limited Data ◽  
Neuritic Plaques ◽  
Brain Changes

The number of studies that have investigated the neuropathology of mild cognitive impairment (MCI) is small, but growing. In this paper we have restricted our focus to the consideration of the presence and extent of postmortem findings relevant to the neuropathology of Alzheimer's disease. We have drawn from studies that have investigated the postmortem neurobiology of the brains of persons with cognitive function at the interface between unimpaired normal function and mild but definite dementia. The data derived from these studies suggest that i) the brains of persons with MCI evidence significant neuropathological and neurobiological changes relative to those without cognitive impairment; ii) in general, the neuropathological and neurobiological changes are qualitatively similar to those observed in the brains of persons with frank AD-like dementia; and iii) the neuropathological and neurobiological brain changes associated with MCI are quantitatively less than those of persons who meet criteria for dementia. Thus, the available, albeit limited, data suggests that MCI is associated with the early stages of the neurobiological and neuropathological changes that culminate in the florid lesions of AD; including the accumulation of neuritic plaques, neurofibrillary tangles, synaptic and neurotransmitter associated deficits, and significant neuronal cell death.

Increased apoptotic neuronal cell death and cognitive impairment at early phase after traumatic brain injury in aged rats

2012 ◽  
Vol 218 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Tatsuki Itoh ◽  
Motohiro Imano ◽  
Shozo Nishida ◽  
Masahiro Tsubaki ◽  
Nobuyuki Mizuguchi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Death ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Early Phase ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Aged Rats

scholarly journals Synergistic Neuroprotective Effect of Schisandra chinensis and Ribes fasciculatum on Neuronal Cell Death and Scopolamine-Induced Cognitive Impairment in Rats

2019 ◽  
Vol 20 (18) ◽  
pp. 4517
Author(s):  
Eunkuk Park ◽  
Min Jeong Ryu ◽  
Nam Ki Kim ◽  
Mun Hyoung Bae ◽  
Youngha Seo ◽  
...  
Keyword(s):  
Cell Death ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Passive Avoidance ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Schisandra Chinensis ◽  
Maze Test

Mild cognitive impairment (MCI) is considered as a transitional stage between aging and Alzheimer’s disease. In the present study, we examined the protective effect of Schisandra chinensis (SC) and Ribes fasciculatum (RF) on neuronal cell death in vitro and scopolamine-induced cognitive impairment in Sprague Dawley® rats in vivo. A mixture of SC and RF extracts (SC+RF) significantly protected against hydrogen peroxide-induced PC12 neuronal cell death. The neuroprotective effect of SC+RF on scopolamine-induced memory impairment in rats was evaluated using the passive avoidance test and the Morris water maze test. In the passive avoidance test, SC+RF-treated rats showed an increased latency to escape, compared to the scopolamine-treated rats. Moreover, SC+RF treatment significantly reduced escape latency in water maze test, compared to treatment with scopolamine alone. To verify the long-term memory, we performed probe test of water maze test. As a result, rat treated with SC+RF spent more time in the target quadrant. Consistent with enhancement of memory function, the brain derived neurotrophic factor (BDNF) and its downstream molecules (pERK, pATK, and pCREB) are increased in SC+RF treatment in hippocampal area compared with scopolamine treated group. These results suggest that a mixture of SC and RF extracts may be a good therapeutic candidate for preventing mild cognitive impairment.

Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models

2007 ◽  
Vol 58 ◽  
pp. S81
Author(s):  
Minji Kim ◽  
Yoori Choi ◽  
Hye-Sun Kim ◽  
Ki Young Shin ◽  
Eun-Mee Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Cognitive Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Disease Models
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