Evidence map›Paper›PMID 30982132›Full record

ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2019

On the central role of mitochondria dysfunction and oxidative stress in Alzheimer's disease.

Tobore Onojighofia Tobore

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

63 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  4. Therapeutic Effects ofMolecules (Basel, Switzerland) · 2026
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3 more citing papers are in PubMed but not listed here.

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

1 author.

Tobore Onojighofia ToboreJohns Hopkins University, Baltimore, MD, USA. toboregameman@gmail.com.ORCID http://orcid.org/0000-0001-7334-2915

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the commonest cause of dementia, with approximately 5 million new cases occurring annually. Despite decades of research, its complex pathophysiology and etiopathogenesis presents a major hindrance to the development of an effective treatment and prevention strategy. Aging is the biggest risk factor for the development of AD, and the total number of older people in the population is going to significantly increase in the next decades, suggesting that AD incidence and prevalence is likely to increase in the future. This makes the need for a better understanding of the disease to be extremely urgent.

methodsA search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was "(dementia* OR Alzheimer's) AND (pathophysiology* OR pathogenesis)". New key terms were identified (new term included "vitamin D, thyroid hormone, mitochondria dysfunction, oxidative stress, testosterone, estrogen, melatonin, progesterone, luteinizing hormone, amyloid-β (Aβ), and hyperphosphorylated tau"). The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1965, and January 31, 2019. The search was limited to studies published in English and other languages involving both animal and human subjects.

resultsMitochondria dysfunction and oxidative stress play a critical role in AD etiopathogenesis and pathophysiology.

conclusionAD treatment and prevention strategies must be geared towards improving mitochondrial function and attenuating oxidative stress.

Indexed as

Alzheimer DiseaseAnimalsHumansMitochondriaOxidative StressAlpha-synuclein (α-synuclein)Alzheimer’s diseaseAmyloid-β (Aβ)Dementia pathogenesisHyperphosphorylated tauMelatonin and dementiaMitochondria dysfunction and dementiaOxidative stress and dementiaSex hormones and Alzheimer’s diseaseThyroid hormone and dementiaVitamin D and dementia

Identifiers

PMID30982132

What Socratic 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 Socratic graph.