Evidence map›Paper›PMID 29564191›Full record

ReviewCurrent genetic medicine reports2018

Mitochondria and Alzheimer's Disease: the Role of Mitochondrial Genetic Variation.

Perry G Ridge, John S K Kauwe

Open access · hybridAbstract readReview
In one paragraph

Review in Current genetic medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 58 citations in OpenAlex.

  1. Mitochondrial haplogroups, but not heteroplasmy, are associated with midlife cognitive function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  2. Mitochondrial DNA affects tau phosphorylation in aging and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The role of mitochondrial genome abundance in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Exploratory analysis of mtDNA haplogroups in two Alzheimer's longitudinal cohorts.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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 1 country.

Perry G RidgeDepartment of Biology, Brigham Young University, 4102 LSB, Provo, UT 84602 USA.
John S K KauweDepartment of Biology, Brigham Young University, 4102 LSB, Provo, UT 84602 USA.
Brigham Young University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAlzheimer's disease (AD) is the most common form of dementia, affects an increasing number of people worldwide, has a rapidly increasing incidence, and is fatal. In the past several years, significant progress has been made towards solving the genetic architecture of AD, but our understanding remains incomplete and has not led to treatments that either cure or slow disease. There is substantial evidence that mitochondria are involved in AD: mitochondrial functional declines in AD, mitochondrial encoded gene expression changes, mitochondria are morphologically different, and mitochondrial fusion/fission are modified. While a majority of mitochondrial proteins are nuclear encoded and could lead to malfunction in mitochondria, the mitochondrial genome encodes numerous proteins important for the electron transport chain, which if damaged could possibly lead to mitochondrial changes observed in AD. Here, we review publications that describe a relationship between the mitochondrial genome and AD and make suggestions for analysis approaches and data acquisition, from existing datasets, to study the mitochondrial genetics of AD. RECENT

findingsNumerous mitochondrial haplogroups and SNPs have been reported to influence risk for AD, but the majority of these have not been replicated, nor experimentally validated. SUMMARY: The role of the mitochondrial genome in AD remains elusive, and several impediments exist to fully understand the relationship between the mitochondrial genome and AD. Yet, by leveraging existing datasets and implementing appropriate analysis approaches, determining the role of mitochondrial genetics in risk for AD is possible.

Indexed as

Alzheimer’s diseaseMitochondrial cascade hypothesisMitochondrial genetics

Identifiers

PMID29564191
PMCPMC5842281
OpenAlexW2791478504

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.