Evidence map›Paper›PMID 40235958›Full record

ArticleBrain communications2025

Regional brain volume changes in Hakim's disease versus Alzheimer's and mild cognitive impairment.

Shigeki Yamada, Takuya Yuzawa, Hirotaka Ito, Chifumi Iseki, Toshiyuki Kondo, Tomoyasu Yamanaka, Motoki Tanikawa, Tomohiro Otani, Satoshi Ii, Yasuyuki Ohta and 4 more

Abstract read
In one paragraph

Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Shigeki YamadaDepartment of Neurosurgery, Nagoya City University Graduate School of Medical Science, Aichi, 467-8601, Japan.ORCID https://orcid.org/0000-0001-7158-5569
Takuya YuzawaMedical System Research & Development Center, FUJIFILM Corporation, Tokyo, 107-0052, Japan.
Hirotaka ItoMedical System Research & Development Center, FUJIFILM Corporation, Tokyo, 107-0052, Japan.ORCID https://orcid.org/0000-0001-7489-3057
Chifumi IsekiDepartment of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Miyagi, 980-8574, Japan.
Toshiyuki KondoDivision of Neurology and Clinical Neuroscience, Department of Internal Medicine III, Yamagata University School of Medicine, Yamagata, 990-9585, Japan.
Tomoyasu YamanakaDepartment of Neurosurgery, Nagoya City University Graduate School of Medical Science, Aichi, 467-8601, Japan.
Motoki TanikawaDepartment of Neurosurgery, Nagoya City University Graduate School of Medical Science, Aichi, 467-8601, Japan.
Tomohiro OtaniDepartment of Mechanical Science and Bioengineering, Graduate School of Engineering Science, Osaka University, Osaka, 560-8531, Japan.ORCID https://orcid.org/0000-0002-6431-2703
Satoshi IiDepartment of Mechanical Engineering, School of Engineering, Institute of Science Tokyo, Tokyo, 145-0061, Japan.
Yasuyuki OhtaDivision of Neurology and Clinical Neuroscience, Department of Internal Medicine III, Yamagata University School of Medicine, Yamagata, 990-9585, Japan.
Yoshiyuki WatanabeDepartment of Radiology, Shiga University of Medical Science, Shiga, 520-2192, Japan.
Shigeo WadaDepartment of Mechanical Science and Bioengineering, Graduate School of Engineering Science, Osaka University, Osaka, 560-8531, Japan.
Marie OshimaInterfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, Tokyo, 153-8505, Japan.
Mitsuhito MaseDepartment of Neurosurgery, Nagoya City University Graduate School of Medical Science, Aichi, 467-8601, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic normal-pressure hydrocephalus (Hakim's disease) is characterized by ventricular enlargement and disproportionately enlarged subarachnoid space hydrocephalus, leading to localized brain deformation. Differentiating regional brain volume changes in Hakim's disease from those in Alzheimer's disease, Hakim's disease with Alzheimer's disease, and mild cognitive impairment provides insights into disease-specific mechanisms. This study aimed to identify disease-specific patterns of brain volume changes in Hakim's disease, Alzheimer's disease, Hakim's disease with Alzheimer's disease, and mild cognitive impairment and compare them with those in cognitively healthy individuals using an advanced artificial intelligence-based brain segmentation tool. The study included 970 participants, comprising 52 patients with Hakim's disease, 256 with Alzheimer's disease, 25 with Hakim's disease with Alzheimer's disease, 163 with mild cognitive impairment, and 474 healthy controls. The intracranial spaces were segmented into 100 brain and 7 CSF subregions from 3D T1-weighted MRIs using brain subregion analysis. The volume ratios of these regions were compared among the groups using Glass's Δ, referencing 400 healthy controls aged ≥50 years. Hakim's disease exhibited significant volume reduction in the supramarginal gyrus of the parietal lobe and the paracentral gyrus of the frontal lobe. Alzheimer's disease exhibited prominent volume loss in the hippocampus and temporal lobe, particularly in the entorhinal cortex, fusiform gyrus, and inferior temporal gyrus. Hakim's disease with Alzheimer's disease showed significant volume reductions in the supramarginal gyrus of the parietal lobe, similar to Hakim's disease, whereas temporal lobe volumes were relatively preserved compared with those in Alzheimer's disease. Patients with mild cognitive impairment aged ≥70 years had comparable regional brain volume ratios with healthy controls in the same age group. The Hakim's disease and Hakim's disease with Alzheimer's disease groups were characterized by volume reductions in the frontal and parietal lobes caused by disproportionately enlarged subarachnoid space hydrocephalus-related compression compared with temporal lobe atrophy observed in the Alzheimer's disease group. These disease-specific morphological changes highlight the need for longitudinal studies to clarify the causes of compression and atrophy.

Indexed as

Alzheimer’s diseaseartificial intelligenceHakim’s diseaseidiopathic normal-pressure hydrocephalusmild cognitive impairment

Identifiers

PMID40235958
PMCPMC11997787

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.