Accelerated long‐term forgetting is a BACE1 inhibitor‐reversible incipient cognitive phenotype in Alzheimer’s disease model mice

Ohno, Minoru

doi:10.1002/npr2.12174

Cited by 8 publications

(10 citation statements)

References 31 publications

(60 reference statements)

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“…More recently and in line with previous research, Ohno (2021) has provided experimental evidence of ALF as a sensitive measure of memory for assessing the effects of antiamyloid treatment in young (4-month-old) AD transgenic mice. While untreated control mice were able to form and initially retain contextual fear memories but lost these memories at an accelerated rate over 28 days, mice pretreated with a β-secretase inhibitor showed almost complete normalization of their long-term forgetting rate.…”

Section: The Phenomenon Of Alfsupporting

confidence: 68%

“…While untreated control mice were able to form and initially retain contextual fear memories but lost these memories at an accelerated rate over 28 days, mice pretreated with a β-secretase inhibitor showed almost complete normalization of their long-term forgetting rate. Although trials of β-secretase inhibitors in humans have not yet shown clinical efficacy in AD (Hampel et al, 2021; Ohno, 2021), the results of the animal research reinforce the idea that intervening at earlier disease stages, and using more sensitive cognitive measures such as ALF, may be necessary to observe behavioral effects.…”

Section: The Phenomenon Of Alfmentioning

confidence: 89%

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A review of accelerated long-term forgetting in Alzheimer’s disease: Current situation and prospects.

García-Martínez¹,

Sánchez‐Juan²,

Butler³

2023

Neuropsychology

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Objective: Advances in our understanding of the Alzheimer’s disease (AD) continuum through in vivo biomarkers have highlighted the need to develop neuropsychological tests that are more sensitive to subtle cognitive changes in the preclinical stages of the disease. Recent data suggest that the assessment of memory retention over extended delays, to detect so-called accelerated long-term forgetting (ALF), may be a reliable way to discriminate between presymptomatic AD and healthy aging. This review aims to present the scientific evidence published to date on this particular aspect of memory. Method: A comprehensive review of all published articles on ALF in AD to the present day. Results: We present findings relating to ALF in neurological disease, discuss theoretical aspects related to the integration of the concept of ALF in the framework of memory models, explain mechanisms that may be involved in its genesis and present supportive work from research in animal models. We focus particularly on aspects relevant to the assessment of ALF in clinical practice. Conclusions: Despite many advances, further research will be needed to define more precisely what ALF is, what neural structures and mechanisms are involved in its occurrence, whether there are distinct patterns of forgetting according to etiology, and when and how to detect ALF most reliably.

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Section: The Phenomenon Of Alfsupporting

confidence: 68%

Section: The Phenomenon Of Alfmentioning

confidence: 89%

A review of accelerated long-term forgetting in Alzheimer’s disease: Current situation and prospects.

García-Martínez¹,

Sánchez‐Juan²,

Butler³

2023

Neuropsychology

View full text Add to dashboard Cite

show abstract

“…AD is also described by the gradual formation of insoluble amyloid plaques and the deposition of amyloid beta-peptide in the brain [27]. Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is a potent drug target for the treatment of AD as prolonged inhibition of BACE1 restricts the structural and functional synaptic plasticity in rats (altering the metabolism of BACE1 substrates) [28,29]. The memory-boosting action of E. prostrata is also supported by its BACE 1 inhibiting property.…”

Section: Discussionmentioning

confidence: 99%

Memory enhancing potential of Euphorbia prostrata through antioxidant, anti-inflammatory, and anti acetylcholinesterase effect against Scopolamine -induced Alzheimer’s disease in Wistar albino rats

Yadav¹,

Yadav²

2023

jrp

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Alzheimer's disease (AD) is an irreversible multi-factorial disease that marks the most common neurodegenerative disorder in the elderly population having cognitive decline as a primary clinical attribute. The present study pursued the evaluation of Euphorbia prostrata (E. prostrata) against scopolamine-induced Alzheimer's disease in Wistar albino rats. Total five groups of animals (having 90 rats) were included in the present study to access the therapeutic impact of E. prostrata. Morris water maze, radial arm maze, and elevated plus maze were evaluated for estimating learning and memory activity. The diverse parameters including oxidative stress, inflammatory cytokines, and acetylcholinesterase assay were assessed to estimate the mechanism of action. The consequences of the present investigation revealed the development of experimental dementia by administration of scopolamine. Whereas the treatment of E. prostrata (100 and 200 mg/kg, per oral (p.o.) and donepezil (1 mg/kg, p.o.) significantly improved the learning and memory ability in scopolamine treated rats. Incomparable to donepezil, the treatment of a higher dose of E. prostrata (200 mg/kg, p.o.) was more effective than compared to the low dose of E. prostrata (100 mg/kg, p.o.). Treatment of donepezil and a higher dose of E. prostrata (200 mg/kg, p.o.) produced comparable results for antiinflammatory, anti-oxidative, and anti-acetylcholinesterase activity. The outcomes of the present investigation showed the memory-enhancing activity of E. prostrata (100 and 200 mg/kg, p.o.) against scopolamine-induced amnesia in rats. This effect of E. prostrata may be due to the inhibition of brain acetylcholinesterase activity, through the involvement of an anti-inflammatory pathway and due to its antioxidant potential.

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“…A low concentration of occludin may cause the BBB to be more permeable [73], causing the upregulation of BACE1 enzymes in the brain. BACE1, in turn, may activate several underlying mediators that result in neuronal apoptosis and memory impairments [74]. Along with this, TNF-α is associated with hippocampal-dependent memory in the brain.…”

Section: The Interplay Between Obesity Oxidative Stress Inflammation ...mentioning

confidence: 99%

The Role of Oxidative Stress and Inflammation in Obesity and Its Impact on Cognitive Impairments—A Narrative Review

et al. 2023

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Obesity is a chronic low-grade inflammatory condition that induces the generation of oxidative stress and inflammation. This oxidative stress and inflammation stimulate brain atrophy and some morphological changes in the brain that eventually result in cognitive impairments. However, there is no exact study that has summarized the role of oxidative stress and inflammation in obesity and its impact on cognitive impairments. Thus, the objective of this review is to recapitulate the current role of oxidative stress and inflammation in cognitive decline based on in vivo evidence. A comprehensive search was performed in Nature, Medline and Ovid, ScienceDirect, and PubMed, and the search was limited to the past 10 years of publication. From the search, we identified 27 articles to be further reviewed. The outcome of this study indicates that a greater amount of fat stored in individual adipocytes in obesity induces the formation of reactive oxygen species and inflammation. This will lead to the generation of oxidative stress, which may cause morphological changes in the brain, suppress the endogenous antioxidant system, and promote neuroinflammation and, eventually, neuronal apoptosis. This will impair the normal function of the brain and specific regions that are involved in learning, as well as memory. This shows that obesity has a strong positive correlation with cognitive impairments. Hence, this review summarizes the mechanism of oxidative stress and inflammation that induce memory loss based on animal model evidence. In conclusion, this review may serve as an insight into therapeutic development focusing on oxidative stress and inflammatory pathways to manage an obesity-induced cognitive decline in the future.

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Accelerated long‐term forgetting is a BACE1 inhibitor‐reversible incipient cognitive phenotype in Alzheimer’s disease model mice

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 8 publications

References 31 publications

A review of accelerated long-term forgetting in Alzheimer’s disease: Current situation and prospects.

A review of accelerated long-term forgetting in Alzheimer’s disease: Current situation and prospects.

Memory enhancing potential of Euphorbia prostrata through antioxidant, anti-inflammatory, and anti acetylcholinesterase effect against Scopolamine -induced Alzheimer’s disease in Wistar albino rats

The Role of Oxidative Stress and Inflammation in Obesity and Its Impact on Cognitive Impairments—A Narrative Review

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