Post-Ischemic Neurodegeneration of the Hippocampus Resembling Alzheimer’s Disease Proteinopathy

Pluta, Ryszard; Januszewski, Sławomir; Czuczwar, Stanisław J.

doi:10.3390/ijms23010306

Cited by 6 publications

(6 citation statements)

References 135 publications

(329 reference statements)

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“…Cerebral ischemia of 3 and 10 min in rodents can induce changes in the hippocampus. [ 53 ] Global cerebral ischemia increases the number of degenerating neurons in the subiculum and CA1 areas and decreases the number of live neurons in the subiculum and CA1 in the hippocampus region with neuronal nuclear protein (NeuN) staining, a robust marker for identification of live neurons. [ 54,55 ] It is reported that cerebral ischemia in rats decreases the number of cells with immunoreactive NeuN in the cortex and striatum.…”

Section: Resultsmentioning

confidence: 99%

“…[ 59 ] It is reported that the accumulation of β‐amyloid after ischemia in the hippocampus is responsible for the secondary degenerative processes, which results in pyramidal neuron death. [ 53 ] Cerebral ischemia induces the accumulation of both Aβ1–40 and β1–42 in the human hippocampus. [ 60 ] In addition, middle cerebral artery occlusion enhanced accumulation of β‐amyloid in the hippocampus of aged rats.…”

Section: Resultsmentioning

confidence: 99%

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Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Noorgaldi,

Sarkala,

Enayati

et al. 2023

Archiv der Pharmazie

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Stroke is the most common cause of death among neurological diseases. The protective effects of Potentilla reptans L. include antioxidative, anti‐inflammatory, and antiapoptotic effects. In this study, the brain protection and beta‐amyloid effects of P. reptans root extract were investigated in the rat brain ischemia/reperfusion (IR) model. Forty male Wistar rats were randomly divided into five groups (n = 8), including IR, sham, and three groups receiving P. reptans with concentrations of 0.025, 0.05, and 0.1 (g/kg/b.w.), which were injected daily for 7 days. For the IR model, the common carotid artery was occluded bilaterally for 8 min. All injections were intraperitoneal (IP). The shuttle box test was used to measure passive avoidance memory. Then the brain tissue was extracted for the histological examination of neuron counts and β‐amyloid plaques using a morphometric technique, and finally, Statistical Package for the Social Sciences software was used for statistical analysis of the data. Pretreatment with P. reptans improved memory impairment. Also, by examining the tissues of the CA1, CA3, and dentate gyrus areas of the hippocampus, it was observed that the number of plaques in the groups receiving P. reptans extract was reduced compared to the IR group, especially at the concentration of 0.05 g/kg/b.w. Also, P. reptans improved the number of neurons at all concentrations, in which the concentration of 0.05 g/kg/b.w. showed more effective therapeutic results. Taken together, we found that P. reptans root extract has beneficial effects on memory impairment, neuronal loss, and β‐amyloid accumulation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Noorgaldi,

Sarkala,

Enayati

et al. 2023

Archiv der Pharmazie

View full text Add to dashboard Cite

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“…Any of these biological changes can affect cerebral autoregulation of blood vessels and result in local or global chronic cerebral hypoperfusion, white matter ischemic changes, and subsequent brain atrophy. 16 , 53 …”

Section: Discussionmentioning

confidence: 99%

“… 12 , 13 There is long‐standing literature on the selective vulnerability of the hippocampus to hypoxia/ischemia and chronic hypoperfusion in both preclinical and clinical studies. 14 , 15 , 16 Furthermore, several studies have shown that cerebrovascular disease MRI markers are associated with hippocampal and medial temporal brain volumes. 17 , 18 , 19 , 20 , 21 Despite this, very few autopsy‐based studies have examined the relationship between measures of intracranial atherosclerosis and MRI‐based measures of Alzheimer's dementia.…”

mentioning

confidence: 99%

Atherosclerosis and Hippocampal Volumes in Older Adults: The Role of Age and Blood Pressure

Kapasi,

Capuano,

Lamar

et al. 2024

JAHA

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Background Lower hippocampal volume is associated with late‐life cognitive decline and is an important, but nonspecific marker for clinical Alzheimer's dementia. Cerebrovascular disease may also be associated with hippocampal volume. Here we study the role of intracranial large vessel disease (atherosclerosis) in association with hippocampal volume and the potential role of age, average late‐life blood pressure across all visits, and other factors (sex, apolipoprotein ε4 [ APOE ε4], and diabetes). Methods and Results Data came from 765 community‐based older people (91 years old on average at death; 72% women), from 2 ongoing clinical‐pathologic cohort studies. Participants completed baseline assessment, annual standardized blood pressure measurements, vascular risk assessment for diabetes, and blood draws to determine APOE genotype, and at death, brains were removed and underwent ex vivo magnetic resonance imaging and neuropathologic evaluation for atherosclerosis pathology and other cerebrovascular and neurodegenerative pathologies. Linear regression models examined the association of atherosclerosis and hippocampal to hemisphere volume ratio and whether age at death, blood pressure, and other factors modified associations. In linear regression models adjusted for demographics and neurodegenerative and other cerebrovascular pathologies, atherosclerosis severity was associated with a lower hippocampal to hemisphere volume ratio. In separate models, we found the effect of atherosclerosis on the ratio of hippocampal to hemisphere volume was attenuated among advanced age at death or having higher systolic blood pressure (interaction terms P ≤0.03). We did not find confounding or interactions with sex, diabetes, or APOE ε4. Conclusions Atherosclerosis severity is associated with lower hippocampal volume, independent of neurodegenerative and other cerebrovascular pathologies. Higher systolic blood pressures and advanced age attenuate associations.

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“…The development of neuroinflammatory lesions has been shown to play a key role in the progression of post-ischemic brain neurodegeneration [ 39 , 44 , 48 ]. Amyloid processing, tau protein modification, autophagy and mitophagy genes are involved in post-ischemic neurodegeneration in the same way as in Alzheimer’s disease [ 40 , 42 , 49 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 ].…”

Section: Molecular Hydrogen Neuroprotection In Post-ischemic Brain In...mentioning

confidence: 99%

Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?

Pluta

Januszewski

Czuczwar

2022

IJMS

Self Cite

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Currently, there is a lot of public interest in naturally occurring substances with medicinal properties that are minimally toxic, readily available and have an impact on health. Over the past decade, molecular hydrogen has gained the attention of both preclinical and clinical researchers. The death of pyramidal neurons in especially the CA1 area of the hippocampus, increased permeability of the blood-brain barrier, neuroinflammation, amyloid accumulation, tau protein dysfunction, brain atrophy, cognitive deficits and dementia are considered an integral part of the phenomena occurring during brain neurodegeneration after ischemia. This review focuses on assessing the current state of knowledge about the neuroprotective effects of molecular hydrogen following ischemic brain injury. Recent studies in animal models of focal or global cerebral ischemia and cerebral ischemia in humans suggest that hydrogen has pleiotropic neuroprotective properties. One potential mechanism explaining some of the general health benefits of using hydrogen is that it may prevent aging-related changes in cellular proteins such as amyloid and tau protein. We also present evidence that, following ischemia, hydrogen improves cognitive and neurological deficits and prevents or delays the onset of neurodegenerative changes in the brain. The available evidence suggests that molecular hydrogen has neuroprotective properties and may be a new therapeutic agent in the treatment of neurodegenerative diseases such as neurodegeneration following cerebral ischemia with progressive dementia. We also present the experimental and clinical evidence for the efficacy and safety of hydrogen use after cerebral ischemia. The therapeutic benefits of gas therapy open up new promising directions in breaking the translational barrier in the treatment of ischemic stroke.

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Post-Ischemic Neurodegeneration of the Hippocampus Resembling Alzheimer’s Disease Proteinopathy

Cited by 6 publications

References 135 publications

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Atherosclerosis and Hippocampal Volumes in Older Adults: The Role of Age and Blood Pressure

Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?

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