Memory impairment was ameliorated by corticolimbic microinjections of arachidonylcyclopropylamide (ACPA) and miRNA-regulated lentiviral particles in a streptozotocin-induced Alzheimer's rat model

Hosseininia, Mohammad; Rostami, Fatemeh; Delphi, Ladan; Ghasemzadeh, Zahra; Kouhkan, Fatemeh; Rezayof, Ameneh

doi:10.1016/j.expneurol.2023.114560

Cited by 6 publications

(2 citation statements)

References 72 publications

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“…This led to a reduction in oxidative stress through the BDNF/TrkB/Akt pathway. In an attempt to enhance memory function, co-administration of ACPA and miRNA-137/-let-7a lentiviral particles was explored, resulting in increased endocannabinoids via induction of the MAGL gene [39]. Additionally, ACEA, AEA, and HU-210 showed significant memory function improvement in AD-mice across several studies [36,37,40,41,45], emphasizing the direct correlation between CB1R and memory function, as underscored in [45], consistent with other findings.…”

Section: Discussionsupporting

confidence: 74%

“…In their study, Hosseininia et al [39] investigated the impact of chronic corticolimbic microinjection of the selective CB1R agonist arachidonylcyclopropylamide (ACPA; 10 ng/0.5 μl) and lentiviral particles containing miRNA-137 (miR-137) or miR-let-7a on memory-impaired animal models exposed to i.c.v. STZ.…”

Section: Selective Agonists Of Cannabinoid Receptor 1 (Cb1r)mentioning

confidence: 99%

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A Comprehensive Exploration of the Multifaceted Neuroprotective Role of Cannabinoids in Alzheimer's Disease Across a Decade of Research

Tyrakis,

Agridi,

Kourti

2024

Preprint

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Alzheimer's disease (AD), a progressive neurodegenerative disorder, manifests through dysregulation of brain function and subsequent loss of bodily control, attributed to β-amyloid plaque deposition and TAU protein hyperphosphorylation and aggregation, leading to neuronal death. Concurrently, similar cannabinoids to the ones derived from Cannabis sativa are present in the endocannabinoid system, acting through receptors CB1R and CB2R and other related receptors such as Trpv-1 and GPR-55, and are being extensively investigated for AD therapy. Given the limited efficacy and adverse effects of current available treatments, alternative approaches are crucial. Therefore, this review aims to identify effective natural and synthetic cannabinoids and elucidate their beneficial actions for AD treatment. PubMed and Scopus databases were queried (2014–2024) using keywords such as "Alzheimer's disease" and "cannabinoids". The majority of natural (THC, CBD, AEA, etc.) and synthetic (JWH-133, WIN55,212-2, CP55-940, etc.) cannabinoids included, showed promise in improving memory, cognition, and behavioral symptoms, potentially via pathways involving antioxidant effects of selective CB1R agonists (such as the BDNF/TrkB/Akt pathway) and immunomodulatory effects of selective CB2R agonists (TLR4/NF-κB p65 pathway). Combining anticholinesterase properties with cannabinoid moiety may enhance therapeutic responses, addressing cholinergic deficits of AD brains. Thus, the positive outcomes of the majority of studies discussed supports further advancing cannabinoids in clinical trials for AD treatment.

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Section: Discussionsupporting

confidence: 74%

Section: Selective Agonists Of Cannabinoid Receptor 1 (Cb1r)mentioning

confidence: 99%

A Comprehensive Exploration of the Multifaceted Neuroprotective Role of Cannabinoids in Alzheimer's Disease Across a Decade of Research

Tyrakis,

Agridi,

Kourti

2024

Preprint

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The role of glutamate NMDA receptors of the mediodorsal thalamus in scopolamine-induced amnesia in rats

Khesmakhi,

Salimi,

Pourmotabbed

et al. 2024

Neuroscience Letters

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40 Hz light preserves synaptic plasticity and mitochondrial function in Alzheimer’s disease model

Barzegar Behrooz,

Aghanoori,

Nazari

et al. 2024

Sci Rep

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Alzheimer’s disease (AD) is the most prevalent type of dementia. Its causes are not fully understood, but it is now known that factors like mitochondrial dysfunction, oxidative stress, and compromised ion channels contribute to its onset and progression. Flickering light therapy has shown promise in AD treatment, though its mechanisms remain unclear. In this study, we used a rat model of streptozotocin (STZ)-induced AD to evaluate the effects of 40 Hz flickering light therapy. Rats received intracerebroventricular (ICV) STZ injections, and 7 days after, they were exposed to 40 Hz flickering light for 15 min daily over seven days. Cognitive and memory functions were assessed using Morris water maze, novel object recognition, and passive avoidance tests. STZ-induced AD rats exhibited cognitive decline, elevated reactive oxygen species, amyloid beta accumulation, decreased serotonin and dopamine levels, and impaired mitochondrial function. However, light therapy prevented these effects, preserving cognitive function and synaptic plasticity. Additionally, flickering light restored mitochondrial metabolites and normalized ATP-insensitive mitochondrial calcium-sensitive potassium (mitoBKCa) channel activity, which was otherwise downregulated in AD rats. Our findings suggest that 40 Hz flickering light therapy could be a promising treatment for neurodegenerative disorders like AD by preserving synaptic and mitochondrial function. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-024-78528-7.

show abstract

Memory impairment was ameliorated by corticolimbic microinjections of arachidonylcyclopropylamide (ACPA) and miRNA-regulated lentiviral particles in a streptozotocin-induced Alzheimer's rat model

Cited by 6 publications

References 72 publications

A Comprehensive Exploration of the Multifaceted Neuroprotective Role of Cannabinoids in Alzheimer's Disease Across a Decade of Research

A Comprehensive Exploration of the Multifaceted Neuroprotective Role of Cannabinoids in Alzheimer's Disease Across a Decade of Research

The role of glutamate NMDA receptors of the mediodorsal thalamus in scopolamine-induced amnesia in rats

40 Hz light preserves synaptic plasticity and mitochondrial function in Alzheimer’s disease model

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