Reduced biophotonic activities and spectral blueshift in Alzheimer's disease and vascular dementia models with cognitive impairment.

Frontiers in aging neuroscience · 2023 · Unclear · Insufficient evidence

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UnclearInsufficient evidencePaper 6776

Glutamate-induced biophotonic activities were significantly reduced and showed a spectral blueshift in synaptosomes and brain slices from AD and VaD model animals. These changes were partially reversed by pre-perfusion with ifenprodil, a GluN2B-containing NMD…

Study snapshot

PublicationFrontiers in aging neuroscience · 2023

Study typeanimal

Reported directionUnclear

Evidence ratingInsufficient

Abstract

BACKGROUND: Although clinically, Alzheimer's disease (AD) and vascular dementia (VaD) are the two major types of dementia, it is unclear whether the biophotonic activities associated with cognitive impairments in these diseases share common pathological features. METHODS: We used the ultraweak biophoton imaging system (UBIS) and synaptosomes prepared by modified percoll method to directly evaluate the functional changes in synapses and neural circuits in AD and VaD model animals. RESULTS: We found that biophotonic activities induced by glutamate were significantly reduced and spectral blueshifted in synaptosomes and brain slices. These changes could be partially reversed by pre-perfusion of the ifenprodil, a specific antagonist of the GluN2B subunit of N-methyl-D-aspartate receptors (NMDARs). CONCLUSION: Our findings suggest that AD and VaD pathology present similar but complex changes in biophotonic activities and transmission at synapses and neural circuits, implying that communications and information processing of biophotonic signals in the brain are crucial for advanced cognitive functions.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typeanimal

Effect directionunclear

PopulationAD and VaD model animals

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthInsufficientConfidence: 74% · Peer reviewed: yes

Main findings

Outcomes measured

Glutamate-induced biophotonic activity in synaptosomes and brain slices
Spectral shift (blueshift) of biophotonic emissions
Reversibility of changes with ifenprodil (GluN2B antagonist)

Limitations

Sample size not reported in abstract
Specific animal models and experimental conditions not detailed in abstract
Not an EMF exposure study; focuses on endogenous ultraweak biophoton signals

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": null,
    "source": null,
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    "sar_wkg": null,
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  },
  "population": "AD and VaD model animals",
  "sample_size": null,
  "outcomes": [
    "Glutamate-induced biophotonic activity in synaptosomes and brain slices",
    "Spectral shift (blueshift) of biophotonic emissions",
    "Reversibility of changes with ifenprodil (GluN2B antagonist)"
  ],
  "main_findings": "Glutamate-induced biophotonic activities were significantly reduced and showed a spectral blueshift in synaptosomes and brain slices from AD and VaD model animals. These changes were partially reversed by pre-perfusion with ifenprodil, a GluN2B-containing NMDAR antagonist.",
  "effect_direction": "unclear",
  "limitations": [
    "Sample size not reported in abstract",
    "Specific animal models and experimental conditions not detailed in abstract",
    "Not an EMF exposure study; focuses on endogenous ultraweak biophoton signals"
  ],
  "evidence_strength": "insufficient",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "Alzheimer's disease",
    "vascular dementia",
    "biophoton imaging",
    "ultraweak biophoton imaging system",
    "synaptosomes",
    "glutamate",
    "spectral blueshift",
    "NMDAR",
    "GluN2B",
    "ifenprodil",
    "synapses",
    "neural circuits",
    "cognitive impairment"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.3389/fnagi.2023.1208274
PubMed: 37727319

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