Evidence map›Paper›PMID 33719595›Full record

ReviewAmerican journal of Alzheimer's disease and other dementias

Therapeutic Potential of Neu1 in Alzheimer's Disease Via the Immune System.

Aiza Khan, Sumit Das, Consolato Sergi

Open access · goldAbstract readReview
In one paragraph

Review in American journal of Alzheimer's disease and other dementias. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Aiza KhanSection of Pediatric Pathology, Department of Laboratory Medicine and Pathology, 3158University of Alberta and Stollery Children's Hospital, Edmonton, Alberta, Canada.
Sumit DasSection of Neuropathology, Department of Laboratory Medicine and Pathology, University of Alberta and Stollery Children's Hospital, Edmonton, Alberta, Canada.ORCID 0000-0002-1826-9644
Consolato SergiSection of Pediatric Pathology, Department of Laboratory Medicine and Pathology, 3158University of Alberta and Stollery Children's Hospital, Edmonton, Alberta, Canada.
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is pathologically characterized by the accumulation of soluble oligomers causing extracellular beta-amyloid deposits in form of neuritic plaques and tau-containing intraneuronal neurofibrillary tangles in brain. One proposed mechanism explaining the formation of these proteins is impaired phagocytosis by microglia/macrophages resulting in defective clearance of soluble oligomers of beta-amyloid stimulating aggregation of amyloid plaques subsequently causing AD. However, research indicates that activating macrophages in M2 state may reduce toxic oligomers. NEU1 mutation is associated with a rare disease, sialidosis. NEU1 deficiency may also cause AD-like amyloidogenic process. Amyloid plaques have successfully been reduced using NEU1.Thus, NEU1 is suggested to have therapeutic potential for AD, with lysosomal exocytosis being suggested as underlying mechanism. Studies however demonstrate that NEU1 may activate macrophages in M2 state, which as noted earlier, is crucial to reducing toxic oligomers. In this review, authors discuss the potential therapeutic role of NEU1 in AD via immune system.

Indexed as

Alzheimer DiseaseNeuraminidaseAmyloid beta-PeptidesBrainHumansImmune SystemPlaque, AmyloidAmyloid beta-PeptidesNEU1 protein, humanNeuraminidaseAlzheimer’simmune systemNeu1neuroinflammationpathophysiology

Identifiers

PMID33719595
PMCPMC10624071
OpenAlexW3137177998

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.