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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–22 of 22 studies by Portelius E · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Other authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

CSF and blood biomarkers for the diagnosis of Alzheimer's disease: a systematic review and meta-analysis

✓ Peer-reviewed alzhub usefulness score 81 out of 100. The Lancet. Neurology 2016-04-08

The core biomarkers differentiated Alzheimer's disease from controls with good performance: CSF T-tau (average ratio 2·54, 95% CI 2·44-2·64, p Interpretation The core CSF biomarkers of neurodegeneration (T-tau, P-tau, and Aβ42), CSF NFL, and plasma T-tau were strongly associated with Alzheimer's disease and the core biomarkers were strongly associated with mild cognitive impairment due to Alzheimer's disease. 2 key findings →

Design: systematic review Participants: 699 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Association of Cerebrospinal Fluid Neurofilament Light Protein Levels With Cognition in Patients With Dementia, Motor Neuron Disease, and Movement Disorders

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA neurology 2019-03-01

Cognitive testing follow-up occurred for 1 to 18 years (mean [SD], 0.98 [2.25] years); autopsy-verified diagnoses were available for 120 of 845 participants with diseases (14.2%). 2 key findings →

Design: case-control study Participants: 913 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Association of Cerebrospinal Fluid Neurofilament Light Concentration With Alzheimer Disease Progression

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA neurology 2016-01-01

Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →

Design: longitudinal study Participants: 95 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Cerebrospinal fluid tau, neurogranin, and neurofilament light in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. EMBO molecular medicine 2016-10-04

Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →

Design: longitudinal study Participants: 93 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Increased CSF neurogranin concentration is specific to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Neurology 2016-01-29

An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50). 1 key finding →

Design: retrospective cohort Participants: 19 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Cerebrospinal fluid neurogranin: relation to cognition and neurodegeneration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain : a journal of neurology 2015-09-15

Cerebrospinal fluid neurogranin was increased in patients with Alzheimer's disease dementia (P < 0.001), progressive mild cognitive impairment (P < 0.001) and stable mild cognitive impairment (P < 0.05) compared with controls, and in Alzheimer's disease dementia (P < 0.01) and progressive mild cognitive impairment (P < 0.05) compared with stable mild cognitive impairment. 2 key findings →

Design: longitudinal study Participants: 95 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2020-07-10

A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Cerebrospinal fluid neurogranin concentration in neurodegeneration: relation to clinical phenotypes and neuropathology

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2018-04-26

Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →

Participants: 915 Evidence: low

Full summary, score breakdown and related studies → Original source

A novel Abeta isoform pattern in CSF reflects gamma-secretase inhibition in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's research & therapy 2010-03-29

CSF Abeta1-14, Abeta1-15, and Abeta1-16 increase during gamma-secretase inhibitor treatment in AD, even at doses that do not affect Abeta1-42 or Abeta1-40, probably because of increased substrate availability of the C99 APP stub (APP beta-CTF) induced by gamma-secretase inhibition. 2 key findings →

Participants: 35 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

C-terminal neurogranin is increased in cerebrospinal fluid but unchanged in plasma in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2015-06-16

This study strengthens the potential of neurogranin as an AD CSF biomarker, which now needs validation in larger studies. 3 key findings →

Participants: 29 Evidence: low

Full summary, score breakdown and related studies → Original source

Cerebrospinal Fluid Amyloid Beta and Tau Concentrations Are Not Modulated by 16 Weeks of Moderate- to High-Intensity Physical Exercise in Patients with Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Dementia and geriatric cognitive disorders 2016-09-20

Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD). 4 key findings →

Participants: 53 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Familial Alzheimer's disease patient-derived neurons reveal distinct mutation-specific effects on amyloid beta

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2019-04-12

Familial Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Phenotypic Screening Identifies Modulators of Amyloid Precursor Protein Processing in Human Stem Cell Models of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Stem cell reports 2017-03-09

Human stem cell models have the potential to provide platforms for phenotypic screens to identify candidate treatments and cellular pathways involved in the pathogenesis of neurodegenerative disorders. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

“Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene-dose-sensitive AD-suppressor in human brain”

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Molecular psychiatry 2020-01-31

A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The aqueous phase of Alzheimer's disease brain contains assemblies built from ∼4 and ∼7 kDa Aβ species

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2015-04-04

Further analysis of brain-derived ∼7 kDa Aβ species, the mechanism by which they assemble and the structures they form should reveal therapeutic and diagnostic opportunities. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

A novel pathway for amyloid precursor protein processing

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neurobiology of aging 2009-07-14

Amyloid precursor protein (APP) can be proteolytically processed along two pathways, the amyloidogenic that leads to the formation of the 40-42 amino acid long Alzheimer-associated amyloid β (Aβ) peptide and the non-amyloidogenic in which APP is cut in the middle of the Aβ domain thus precluding Aβ formation. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A selected reaction monitoring (SRM)-based method for absolute quantification of Aβ38, Aβ40, and Aβ42 in cerebrospinal fluid of Alzheimer's disease patients and healthy controls

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2013-01-01

Cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD) are increasingly used in research centers, clinical trials, and clinical settings. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed