Evidence map›Paper›PMID 32737755›Full record

ArticleReviews of physiology, biochemistry and pharmacology2023

Endosomal Acid-Base Homeostasis in Neurodegenerative Diseases.

Hari Prasad, Rajini Rao

Open access · greenAbstract read
In one paragraph

Article in Reviews of physiology, biochemistry and pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. The Recycling Endosomal (NaActa physiologica (Oxford, England) · 2026
    Article
  4. Article
  5. Alterations in the NaCerebellum (London, England) · 2025
    Article
  6. 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

2 authors at 1 institution in 2 countries.

Hari PrasadDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Rajini RaoDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. rrao@jhmi.edu.
Johns Hopkins University · US

Funding

Transport Mechanism and Renal Function of a Newly Recognized Na+/H+ ExchangerR01DK108304 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2015 to 2019
$2.3M
DBT-Wellcome Trust India Alliance IA/E/17/1/503665NIDDK NIH HHS R01 DK108304Wellcome Trust
6 · The paper itself

Abstract

Neurodegenerative disorders are debilitating and largely untreatable conditions that pose a significant burden to affected individuals and caregivers. Overwhelming evidence supports a crucial preclinical role for endosomal dysfunction as an upstream pathogenic hub and driver in Alzheimer's disease (AD) and related neurodegenerative disorders. We present recent advances on the role of endosomal acid-base homeostasis in neurodegeneration and discuss evidence for converging mechanisms. The strongest genetic risk factor in sporadic AD is the ε4 allele of Apolipoprotein E (ApoE4), which potentiates pre-symptomatic endosomal dysfunction and prominent amyloid beta (Aβ) pathology, although how these pathways are linked mechanistically has remained unclear. There is emerging evidence that the Christianson syndrome protein NHE6 is a prominent ApoE4 effector linking endosomal function to Aβ pathologies. By functioning as a dominant leak pathway for protons, the Na

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesApolipoprotein E4HomeostasisHumansAmyloid beta-PeptidesApolipoprotein E4Alzheimer’s diseaseAmyloidApoE4Endosomal pHNa+/H+ exchangerNHE6

Identifiers

PMID32737755
PMCPMC7614123
OpenAlexW3046616239

What OpenQuestion holds

Textmetadata
LicenceTDM
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.