Evidence map›Paper›PMID 36223647›Full record

ReviewBrain pathology (Zurich, Switzerland)2023

Hypothesis review: Alzheimer's overture guidelines.

Isidro Ferrer

Open access · goldAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Alzheimer's Disease Neuropathological Change in Aged Non-Primate Mammals.International journal of molecular sciences · 2024
    Review
  17. Review
  18. The shift in the fatty acid composition of the circulating lipidome in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    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

1 author at 1 institution in 1 country.

Isidro FerrerDepartment of Pathology and Experimental Therapeutics, University of Barcelona (UB), Barcelona, Spain.ORCID 0000-0001-9888-8754
Biomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

La Caixa Foundation LCF/PR/HR19/52160007: HR18-00452
6 · The paper itself

Abstract

National Institute on Aging-Alzheimer's Association definition and classification of sporadic Alzheimer's disease (sAD) is based on the assumption that β-amyloid drives the pathogenesis of sAD, and therefore, β-amyloid pathology is the sine-qua-non condition for the diagnosis of sAD. The neuropathological diagnosis is based on the concurrence of senile plaques (SPs) and neurofibrillary tangles (NFTs) designated as Alzheimer's disease neuropathological changes. However, NFTs develop in the brain decades before the appearance of SPs, and their distribution does not parallel the distribution of SPs. Moreover, NFTs are found in about 85% of individuals at age 65 and around 97% at age 80. SPs occur in 30% at age 65 and 50%-60% at age 80. More than 70 genetic risk factors have been identified in sAD; the encoded proteins modulate cell membranes, synapses, lipid metabolism, and neuroinflammation. Alzheimer's disease (AD) overture provides a new concept and definition of brain aging and sAD for further discussion. AD overture proposes that sAD is: (i) a multifactorial and progressive neurodegenerative biological process, (ii) characterized by the early appearance of 3R + 4Rtau NFTs, (iii) later deposition of β-amyloid and SPs, (iv) with particular non-overlapped regional distribution of NFTs and SPs, (v) preceded by or occurring in parallel with molecular changes affecting cell membranes, cytoskeleton, synapses, lipid and protein metabolism, energy metabolism, neuroinflammation, cell cycle, astrocytes, microglia, and blood vessels; (vi) accompanied by progressive neuron loss and brain atrophy, (vii) prevalent in human brain aging, and (viii) manifested as pre-clinical AD, and progressing not universally to mild cognitive impairment due to AD, and mild, moderate, and severe AD dementia.

Indexed as

Alzheimer DiseaseAgedAged, 80 and overAmyloid beta-PeptidesBrainHumansNeurofibrillary TanglesNeuroinflammatory DiseasesPlaque, Amyloidtau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer's diseasegeneticshuman brain agingmembranesneurofibrillary tanglesrisk factorssenile plaquestauβ-Amyloid

Identifiers

PMID36223647
PMCPMC9836379
OpenAlexW4304808129

What Socratic 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 Socratic graph.