Evidence map›Paper›PMID 34222873›Full record

ReviewBrain communications2021

The role of the medial prefrontal cortex in cognition, ageing and dementia.

Dan D Jobson, Yoshiki Hase, Andrew N Clarkson, Rajesh N Kalaria

Open access · goldAbstract readReview
In one paragraph

Review in Brain communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed, 6 pooled it
22.6field-weighted citation impact, top 1% 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

184 citing papers in PubMed, 6 syntheses or guidelines pooled it, 316 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Stress, stress systems, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  18. Article
  19. Article
  20. Article

124 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

4 authors at 2 institutions in 2 countries.

Dan D JobsonTranslational and Clinical Research Institute, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK.ORCID https://orcid.org/0000-0003-1151-4827
Yoshiki HaseTranslational and Clinical Research Institute, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK.ORCID https://orcid.org/0000-0002-9538-905X
Andrew N ClarksonDepartment of Anatomy, Brain Health Research Centre and Brain Research New Zealand, University of Otago, Dunedin 9054, New Zealand.ORCID https://orcid.org/0000-0003-3804-3834
Rajesh N KalariaTranslational and Clinical Research Institute, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne NE4 5PL, UK.ORCID https://orcid.org/0000-0001-7907-4923
Newcastle Hospitals - Campus for Ageing and Vitality · GBBrain Research New Zealand · NZ

Funding

Medical Research Council G0400074Medical Research Council G0502157Medical Research Council G0900652Medical Research Council G1100540
6 · The paper itself

Abstract

Humans require a plethora of higher cognitive skills to perform executive functions, such as reasoning, planning, language and social interactions, which are regulated predominantly by the prefrontal cortex. The prefrontal cortex comprises the lateral, medial and orbitofrontal regions. In higher primates, the lateral prefrontal cortex is further separated into the respective dorsal and ventral subregions. However, all these regions have variably been implicated in several fronto-subcortical circuits. Dysfunction of these circuits has been highlighted in vascular and other neurocognitive disorders. Recent advances suggest the medial prefrontal cortex plays an important regulatory role in numerous cognitive functions, including attention, inhibitory control, habit formation and working, spatial or long-term memory. The medial prefrontal cortex appears highly interconnected with subcortical regions (thalamus, amygdala and hippocampus) and exerts top-down executive control over various cognitive domains and stimuli. Much of our knowledge comes from rodent models using precise lesions and electrophysiology readouts from specific medial prefrontal cortex locations. Although, anatomical disparities of the rodent medial prefrontal cortex compared to the primate homologue are apparent, current rodent models have effectively implicated the medial prefrontal cortex as a neural substrate of cognitive decline within ageing and dementia. Human brain connectivity-based neuroimaging has demonstrated that large-scale medial prefrontal cortex networks, such as the default mode network, are equally important for cognition. However, there is little consensus on how medial prefrontal cortex functional connectivity specifically changes during brain pathological states. In context with previous work in rodents and non-human primates, we attempt to convey a consensus on the current understanding of the role of predominantly the medial prefrontal cortex and its functional connectivity measured by resting-state functional MRI in ageing associated disorders, including prodromal dementia states, Alzheimer's disease, post-ischaemic stroke, Parkinsonism and frontotemporal dementia. Previous cross-sectional studies suggest that medial prefrontal cortex functional connectivity abnormalities are consistently found in the default mode network across both ageing and neurocognitive disorders such as Alzheimer's disease and vascular cognitive impairment. Distinct disease-specific patterns of medial prefrontal cortex functional connectivity alterations within specific large-scale networks appear to consistently feature in the default mode network, whilst detrimental connectivity alterations are associated with cognitive impairments independently from structural pathological aberrations, such as grey matter atrophy. These disease-specific patterns of medial prefrontal cortex functional connectivity also precede structural pathological changes and may be driven by ageing-related vascular mechanisms. The default mode network supports utility as a potential biomarker and therapeutic target for dementia-associated conditions. Yet, these associations still require validation in longitudinal studies using larger sample sizes.

Indexed as

ageingdefault mode networkdementiaprefrontal cortexvascular cognitive impairment

Identifiers

PMID34222873
PMCPMC8249104
OpenAlexW3167900828

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.