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Peer-reviewedCC BYAnimals : an open access journal from MDPI

Neurobiology of Pet Loss Grief: A Review from a One Health Perspective.

  1. 1Department of Biochemistry, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Republic of Korea.
  2. 2Section of Molecular and Cellular Medicine, Medical Institute of Dongguk University, Gyeongju 38066, Republic of Korea.

Abstract

The loss of a companion animal can provoke grief whose intensity rivals human bereavement, yet its biological basis remains largely uncharted. This structured narrative review synthesizes neurobiological, endocrinological, immunological, and psychosocial evidence into a mechanistic framework offered not as established fact but as a source of testable hypotheses. We trace the substrates of the human-animal bond across six interacting systems and propose how disruption of each upon an animal's death may drive grief. Three carry comparatively robust analogical support (oxytocinergic signaling, hypothalamic-pituitary-adrenal [HPA] axis regulation, and neuroinflammatory activation) and three are more exploratory (dopaminergic, serotonergic, and endocannabinoid pathways). Integrating extracted study-level data into transparent prioritization heuristics, we identify the HPA axis, assessed with its coupled oxytocinergic partner, as the most defensible first target for a direct biomarker study, a conclusion robust across three methodologically independent analyses. No direct pet-loss evidence yet supports any proposal, and this gap is the review's central motivation. As applied context, we address euthanasia-related guilt, disenfranchised grief under East Asian norms (a tentative "double disenfranchisement" hypothesis that we put forward for testing), assessment instruments, evidence-graded therapies, priorities for developing Korean-language tools, and One Health research priorities.

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BibTeX
@article{ngo2026neurobiology,
  title = {{Neurobiology of Pet Loss Grief: A Review from a One Health Perspective.}},
  author = {Thanh Huu Phan Ngo and Jiwon Oh and Hyeong Jun Kim and Wan Lee},
  journal = {Animals : an open access journal from MDPI},
  year = {2026},
  month = oct,
  doi = {10.3390/ani16193129},
  url = {https://europepmc.org/article/MED/42883098},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Neurobiology of Pet Loss Grief: A Review from a One Health Perspective.
AU  - Thanh Huu Phan Ngo
AU  - Jiwon Oh
AU  - Hyeong Jun Kim
AU  - Wan Lee
PY  - 2026
DA  - 2026/10/06
JO  - Animals : an open access journal from MDPI
DO  - 10.3390/ani16193129
UR  - https://europepmc.org/article/MED/42883098
AB  - The loss of a companion animal can provoke grief whose intensity rivals human bereavement, yet its biological basis remains largely uncharted. This structured narrative review synthesizes neurobiological, endocrinological, immunological, and psychosocial evidence into a mechanistic framework offered not as established fact but as a source of testable hypotheses. We trace the substrates of the human-animal bond across six interacting systems and propose how disruption of each upon an animal's death may drive grief. Three carry comparatively robust analogical support (oxytocinergic signaling, hypothalamic-pituitary-adrenal [HPA] axis regulation, and neuroinflammatory activation) and three are more exploratory (dopaminergic, serotonergic, and endocannabinoid pathways). Integrating extracted study-level data into transparent prioritization heuristics, we identify the HPA axis, assessed with its coupled oxytocinergic partner, as the most defensible first target for a direct biomarker study, a conclusion robust across three methodologically independent analyses. No direct pet-loss evidence yet supports any proposal, and this gap is the review's central motivation. As applied context, we address euthanasia-related guilt, disenfranchised grief under East Asian norms (a tentative "double disenfranchisement" hypothesis that we put forward for testing), assessment instruments, evidence-graded therapies, priorities for developing Korean-language tools, and One Health research priorities.
SN  - 2076-2615
ER  -