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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
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
0.00
Safety concerns
0.00
Off-target
0.00
Trial stage
preclinical
0.90
Pharma competitors
0.00
AE severity
0.00
MOA weight loss
0.00
Endpoints
0.00
Approved
False
0.90