Evidence map›Paper›PMID 34374777›Full record

ArticleJournal of neuropathology and experimental neurology2021

Loss of Lysosomal Proteins Progranulin and Prosaposin Associated with Increased Neurofibrillary Tangle Development in Alzheimer Disease.

Anarmaa Mendsaikhan, Ikuo Tooyama, Geidy E Serrano, Thomas G Beach, Douglas G Walker

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  4. Prosaposin in CNS health and disease, metabolic stress and exercise adaptation.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
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4 · The record

Corrections and comments

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

5 authors at 2 institutions in 2 countries.

Anarmaa MendsaikhanMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan (AM, IT, DGW).
Ikuo TooyamaMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan (AM, IT, DGW).
Geidy E SerranoCivin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona (GES, TGB).
Thomas G BeachCivin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona (GES, TGB).
Douglas G WalkerMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan (AM, IT, DGW).
Shiga University of Medical Science · JPBanner Sun Health Research Institute · US

Funding

National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

Alzheimer disease (AD) is a progressive neurodegenerative disease causing cognitive decline in the aging population. To develop disease-modifying treatments, understanding the mechanisms behind the pathology is important, which should include observations using human brain samples. We reported previously on the association of lysosomal proteins progranulin (PGRN) and prosaposin (PSAP) with amyloid plaques in non-demented aged control and AD brains. In this study, we investigated the possible involvement of PGRN and PSAP in tangle formation using human brain tissue sections of non-demented aged control subjects and AD cases and compared with cases of frontotemporal dementia with granulin (GRN) mutations. The study revealed that decreased amounts of PGRN and PSAP proteins were detected even in immature neurofibrillary tangles, while colocalization was still evident in adjacent neurons in all cases. Results suggest that neuronal loss of PGRN preceded loss of PSAP as tangles developed and matured. The GRN mutation cases exhibited almost complete absence of PGRN in most neurons, while PSAP signal was preserved. Although based on correlative data, we suggest that reduced levels of PGRN and PSAP and their interaction in neurons might predispose to accumulation of p-Tau protein.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBrainFemaleHumansMaleMiddle AgedMutationNeurofibrillary TanglesProgranulinsSaposinsProgranulinsPSAP protein, humanSaposinsAlzheimer diseaseNeuropathologyProgranulinProsaposinTangles

Identifiers

PMID34374777
PMCPMC8433593
OpenAlexW3187931825

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.