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Извлечено: 997 / 997 (100.0%) Средняя confidence: 0.13
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Neurocaf™, A green coffee bean extract containing eicosanoyl-5-hydroxytryptamide and chlorogenic acids enhances cognitive function and neuronal plasticity in a scopolamine-induced amnesia mouse model.

PMID: 41533228 · DOI: 10.1007/s11011-025-01777-6 · Metabolic brain disease, 2026 · Karempudi Venkatakrishna, Kuppam Sundeep, Amritha Raj, Thammatadhahalli Parameshwarappa Prasanna Kumara, Harakanahalli B
📄 Abstract

This study aimed to evaluate the memory health benefits of Neurocaf™, a standardized green coffee bean extract. Neurocaf was characterized for the presence of 5-hydroxytryptamide esters, eicosanoyl-5-hydroxytryptamide (EHT), and chlorogenic acids using HPLC-PDA detector. The inhibitory kinetics of Neurocaf against acetylcholinesterase (AChE) were assessed in vitro. Cognitive efficacy was further investigated in a scopolamine-induced amnesia mouse model. In a 25-day study, male Swiss albino mice (25-30 g) were pretreated orally with Neurocaf (200 or 400 mg/kg body weight) or donepezil (3 mg/kg body weight) for 14 days followed by behavioural assessments and a 7-day co-treatment with scopolamine (0.75 mg/kg, i.p.). Neurocaf exhibited mixed competitive AChE inhibition in vitro (IC₅₀ = 298.4 µg/mL). At 400 mg/kg, it significantly enhanced spatial memory performance, demonstrated by reduced transfer latency in the elevated plus maze (p < 0.01) and decreased escape latency in the Morris water maze (p < 0.001). The extract dose-dependently suppressed brain AChE activity and elevated acetylcholine levels in scopolamine-treated mice. Furthermore, it attenuated oxidative stress, upregulated BDNF/TrkB signaling, modulated apoptotic protein expression (increased Bcl2, decreased Bax), and inhibited caspase activation, offering neuroprotection against scopolamine-induced neuronal damage. These findings highlight the potential memory functions of Neurocaf, supporting its further evaluation as a candidate functional food or dietary supplement for brain health.

Confidence: 0.26 · 13 полей извлечено
Идентификация (6 полей)
Target
Acetylcholinesterase
0.95
Alt. target
AChE
0.95
Protein family
—
0.00
Functional class
—
0.00
Subcellular loc.
—
0.00
Isoforms (metab/obesity)
—
0.00
Механизм действия (21 полей)
Mechanism
Mixed competitive acetylcholinesterase inhibition
0.90
Mutations (obesity/lean)
—
0.00
Activity (obesity)
—
0.00
Activity temporal
—
0.00
Energy balance
—
0.00
Appetite
—
0.00
Fat metabolism
—
0.00
Lipolysis
—
0.00
Thermogenesis
—
0.00
Muscle metabolism
—
0.00
Inflammation
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0.00
Glucose metabolism
—
0.00
AA metabolism
—
0.00
Hormonal pathways
—
0.00
Cell death
Modulates apoptotic protein expression (increased Bcl2, decreased Bax) and inhibits caspase activation, offering neuroprotection
0.90
Adipocyte fibrosis
—
0.00
Upstream (biochem)
—
0.00
Upstream (physiol)
—
0.00
Downstream (biochem)
BDNF/TrkB signaling, Bcl2, Bax, caspases
0.90
Downstream (physiol)
—
0.00
PTMs
—
0.00
Экспрессия (8 полей)
Tissue expression
—
0.00
In vitro
Acetylcholinesterase inhibition assay
0.95
In vivo
Scopolamine-induced amnesia mouse model
0.95
In silico
—
0.00
Genetic association
—
0.00
Ex vivo
—
0.00
Animal model
Male Swiss albino mice
0.95
Diet/model
Scopolamine-induced amnesia model
0.95
Клиника (11 полей)
Drug
Neurocaf™
1.00
Indication
cognitive function and memory health
0.90
Patient subgroups
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0.00
Safety concerns
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0.00
Off-target
—
0.00
Trial stage
preclinical
0.90
Pharma competitors
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0.00
AE severity
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0.00
MOA weight loss
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0.00
Endpoints
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0.00
Approved
False
0.90