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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD) afflicts an estimated 20 million people worldwide and is the fourth-leading cause of death in the developed world. The most common cause of dementia in older individuals, AD is characterized by neuropathologies including synaptic and neuronal degeneration, amyloid plaques, and neurofibrillary tangles (NTFs). Amyloid plaques are primarily composed of amyloid-beta peptide (Aβ), which accumulates in the brains of patients with AD. Further, small aggregates termed Aβ oligomers are implicated in the synaptic loss and neuronal degeneration underlying early cognitive impairments. Whether Aβ accumulates in part because of dysregulated clearance from the brain remains unclear. The flow of substances (e.g., nutrients, drugs, toxins) in and out of the brain is mediated by the blood-brain-barrier (BBB). The BBB exhibits impairment in AD patients and animal models. The effect of BBB impairment on Aβ, and whether BBB function is affected by non-neurological pathologies that impair peripheral clearance requires further investigation. In particular, impaired peripheral clearance is a feature of nonalcoholic fatty liver disease (NAFLD), a spectrum of liver disorders characterized by accumulation of fat in the liver accompanied by varying degrees of inflammation and hepatocyte injury. NAFLD has reached epidemic proportions, with an estimated prevalence between 20% and 30% of the general population. This chronic condition may influence AD pathogenesis. This review article summarizes the current state of the literature linking NAFLD and AD, highlighting the role of the major Aβ efflux and clearance protein, the LRP-1 receptor, which is abundantly expressed in liver, brain, and vasculature.

Key findings

The effect of BBB impairment on Aβ, and whether BBB function is affected by non-neurological pathologies that impair peripheral clearance requires further investigation.
In particular, impaired peripheral clearance is a feature of nonalcoholic fatty liver disease (NAFLD), a spectrum of liver disorders characterized by accumulation of fat in the liver accompanied by varying degrees of inflammation and hepatocyte injury.
NAFLD has reached epidemic proportions, with an estimated prevalence between 20% and 30% of the general population.
This chronic condition may influence AD pathogenesis.
This review article summarizes the current state of the literature linking NAFLD and AD, highlighting the role of the major Aβ efflux and clearance protein, the LRP-1 receptor, which is abundantly expressed in liver, brain, and vasculature.

Study details

Evidence strengthLow

How this study scored 41/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience)
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	2 / 5	2019 — within 10 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	— / 7	No citation count (not found in OpenAlex) — left out of this score
Citations per year	— / 5	No citation count or no year — left out of this score
Impact for its field and year	— / 6	No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here	— / 6	Not yet checked against this library's citation graph — left out of this score
Still being cited	— / 4	No yearly citation counts — left out of this score
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multi-centre collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 31379558)
Free to read	2 / 2	Free to read
Points	24 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100.
Total	41 / 100	—

What each of these 20 components measures, and what this score is not →

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Cite this study APA, Vancouver, BibTeX · download .bib or .ris

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APA 7th

Estrada, L. D., Ahumada, P., Cabrera, D., & Arab, J. P. (2019). Liver Dysfunction as a Novel Player in Alzheimer's Progression: Looking Outside the Brain. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2019.00174

Vancouver

Estrada LD, Ahumada P, Cabrera D, Arab JP. Liver Dysfunction as a Novel Player in Alzheimer's Progression: Looking Outside the Brain. Frontiers in aging neuroscience. 2019. doi:10.3389/fnagi.2019.00174. PMID: 31379558.

BibTeX

@article{estrada2019-31379558,
  author  = {Estrada, L. D. and Ahumada, P. and Cabrera, D. and Arab, J. P.},
  title   = {{Liver Dysfunction as a Novel Player in Alzheimer's Progression: Looking Outside the Brain}},
  journal = {Frontiers in aging neuroscience},
  year    = {2019},
  doi     = {10.3389/fnagi.2019.00174},
  pmid    = {31379558},
  url     = {https://doi.org/10.3389/fnagi.2019.00174}
}

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