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27/100

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Treatments

Topic: Brain proteins, microglia and lab models

Recent progress of pharmacotherapy enabled anti-amyloid and anti-tau immunotherapy for Alzheimer disease. Yet, non-pharmacological factors, alimentation, sleep, exercise, stress-management or cognition stimulation, has also been emphasized. The D-neuron, that is β‐phenylethylamine (PEA) neuron, or TAAR1 ligand neuron, localizes from D1 (spinal cord) to D18 (cerebral cortex) in caudo-rostral order of mammalian brains. In post-mortem brains with schizophrenia, D-neurons lacked in the nucleus accumbens (Acc, D16), a projection field of mesolimbic dopamine system. This lead to establish “D-cell hypothesis of mental illnesses”, and a novel therapy aimed at protection and activation of D-neuron, “D-neuron protection / activation (DPA) therapy”. As histochemical visualization of D-neurons is a no easy technique, D-neuron activity in the CNS should initially be evaluated indirectly by biomarkers, such as PEA, brain-derived neurotrophic factor (BDNF), tyramine, octopamine and β‐endorphin, and biomarkers of inflammation, such as CRP, TNF and IL-6 in cerebrospinal fluid (CSF), serum or urine. Reliable biomarkers of mental / cognitive functions should also be employed. “DPA therapy” is a novel cellular level treatment of neuropsychiatric illnesses including dementia.

Key findings

The D-neuron, that is β‐phenylethylamine (PEA) neuron, or TAAR1 ligand neuron, localizes from D1 (spinal cord) to D18 (cerebral cortex) in caudo-rostral order of mammalian brains.
In post-mortem brains with schizophrenia, D-neurons lacked in the nucleus accumbens (Acc, D16), a projection field of mesolimbic dopamine system.
This lead to establish “D-cell hypothesis of mental illnesses”, and a novel therapy aimed at protection and activation of D-neuron, “D-neuron protection / activation (DPA) therapy”.
As histochemical visualization of D-neurons is a no easy technique, D-neuron activity in the CNS should initially be evaluated indirectly by biomarkers, such as PEA, brain-derived neurotrophic factor (BDNF), tyramine, octopamine and β‐endorphin, and biomarkers of inflammation, such as CRP, TNF and IL-6 in cerebrospinal fluid (CSF), serum or urine.
Reliable biomarkers of mental / cognitive functions should also be employed. “DPA therapy” is a novel cellular level treatment of neuropsychiatric illnesses including dementia.

Why it matters

This paper proposes a 'D-neuron protection / activation' therapy concept for neuropsychiatric illnesses including dementia, based on D-neuron findings in post-mortem schizophrenia brains. It suggests indirect biomarkers for evaluating D-neuron activity but reports no clinical trial or confirmed treatment effect.

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Study details

Evidence strengthLow

How this study scored 27/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Advances in Bioengineering and Biomedical Science Research)
Journal's citation record	0 / 4	Advances in Bioengineering and Biomedical Science Research: journal h-index 5 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	4 / 5	2025 — within 3 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 3 year(s) since 2025
Impact for its field and year	0 / 6	Cited 0.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Keiko Ikemoto: h-index 19 (OpenAlex, whole career)
Institution's track record	1 / 3	The University of Tokyo: institution h-index 1,463 (OpenAlex)
Multi-centre collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	1 / 2	Not in PubMed, but has a DOI
Free to read	2 / 2	Free to read
Total	27 / 100	—

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Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Ikemoto, K. (2025). “D-Neuron Protection / Activation (DPA) Therapy”: New Strategy for Treatment of Neuropsychiatric Illnesses. Advances in Bioengineering and Biomedical Science Research. https://doi.org/10.33140/abbsr.08.01.01

Vancouver

Ikemoto K. “D-Neuron Protection / Activation (DPA) Therapy”: New Strategy for Treatment of Neuropsychiatric Illnesses. Advances in Bioengineering and Biomedical Science Research. 2025. doi:10.33140/abbsr.08.01.01.

BibTeX

@article{ikemoto2025-e8a83631,
  author  = {Ikemoto, Keiko},
  title   = {{“D-Neuron Protection / Activation (DPA) Therapy”: New Strategy for Treatment of Neuropsychiatric Illnesses}},
  journal = {Advances in Bioengineering and Biomedical Science Research},
  year    = {2025},
  doi     = {10.33140/abbsr.08.01.01},
  url     = {https://doi.org/10.33140/abbsr.08.01.01}
}

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