Evidence map›Paper›PMID 34856906›Full record

ArticleCurrent neuropharmacology2022

Current and Near-Future Treatment of Alzheimer's Disease.

Kazimierz Gąsiorowski, Jadwiga Barbara Brokos, Marta Sochocka, Michał Ochnik, Justyna Chojdak-Łukasiewicz, Katarzyna Zajączkowska, Michał Fułek, Jerzy Leszek

Open access · hybridAbstract read
In one paragraph

Article in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Zunyimycin C enhances immunity and improves cognitive impairment and its mechanism.Frontiers in cellular and infection microbiology · 2022
    Article
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

8 authors at 2 institutions in 1 country.

Kazimierz GąsiorowskiDepartment of Basic Medical Sciences, Wrocław Medical University, Wrocław, Poland.
Jadwiga Barbara BrokosDepartment of Basic Medical Sciences, Wrocław Medical University, Wrocław, Poland.
Marta SochockaLaboratory of Virology, Department of Immunology of Infectious Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Michał OchnikLaboratory of Virology, Department of Immunology of Infectious Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Justyna Chojdak-ŁukasiewiczDepartment of Neurology, Wrocław Medical University, Wrocław, Poland.
Katarzyna ZajączkowskaFaculty of Medicine, Wrocław Medical University, Wrocław, Poland.
Michał FułekDepartment of Internal Medicine, Occupational Diseases, Hypertension and Clinical Oncology, Wrocław Medical University, Wrocław, Poland.
Jerzy LeszekDepartment of Psychiatry, Wrocław Medical University, Wrocław, Poland.
Wroclaw Medical University · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings have improved our understanding of the multifactorial nature of AD. While in early asymptomatic stages of AD, increased amyloid-β synthesis and tau hyperphosphorylation play a key role, while in the latter stages of the disease, numerous dysfunctions of homeostatic mechanisms in neurons, glial cells, and cerebrovascular endothelium determine the rate of progression of clinical symptoms. The main driving forces of advanced neurodegeneration include increased inflammatory reactions in neurons and glial cells, oxidative stress, deficiencies in neurotrophic growth and regenerative capacity of neurons, brain insulin resistance with disturbed metabolism in neurons, or reduction of the activity of the Wnt-β catenin pathway, which should integrate the homeostatic mechanisms of brain tissue. In order to more effectively inhibit the progress of neurodegeneration, combination therapies consisting of drugs that rectify several above-mentioned dysfunctions should be used. It should be noted that many widely-used drugs from various pharmacological groups, "in addition" to the main therapeutic indications, have a beneficial effect on neurodegeneration and may be introduced into clinical practice in combination therapy of AD. There is hope that complex treatment will effectively inhibit the progression of AD and turn it into a slowly progressing chronic disease. Moreover, as the mechanisms of bidirectional communication between the brain and microbiota are better understood, it is expected that these pathways will be harnessed to provide novel methods to enhance health and treat AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainHumansNeuronsOxidative StressAmyloid beta-PeptidesAlzheimer’s diseasebrain insulin resistancecombination therapyinflammationoxidative stressWnt-β catenin pathway

Identifiers

PMID34856906
PMCPMC9886829
OpenAlexW3217174241

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.