alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 126–150 of 377 studies with an author at University of Gothenburg (SE) · free to read (page 6 of 16) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 377 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

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

Subjects

Authors

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

Other institutions

From OpenAlex; 17,651 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.

Cerebral Amyloid Angiopathy and Downstream Alzheimer Disease Plasma Biomarkers

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA network open 2025-05-01

Lobar CMB counts and the presence of CAA were associated with downstream AD plasma biomarkers, including p-tau217 (β = 0.12 [95% CI, 0.05-0.18] and 0.29 [95% CI, 0.12-0.47], respectively), GFAP (β = 0.07 [95% CI, 0.03-0.12] and 0.20 [95% CI, 0.09-0.31], respectively), and NfL (β = 0.07 [95% CI, 0.03-0.11] and 0.16 [95% CI, 0.06-0.25], respectively) with and without the mediation of Aβ uptake on PET (indirect effect: lobar CMBs-p-tau217, 59.8% [β = 0.07 (95% CI, 0.03-0.11)]; lobar CMBs-GFAP, 49.3% [β = 0.04 (95% CI, 0.01-0.06)]; lobar CMBs-NfL, 20.9% [β = 0.01 (95% CI, 0.01-0.03)]; CAA-p-tau217, 50.9% [β = 0.15 (95% CI, 0.06-0.24)]; CAA-GFAP, 39.2% [β = 0.08 (95% CI, 0.03-0.13)]; CAA-NfL, 19.2% [β = 0.03 (95% CI, 0.01-0.05)]). 4 key findings →

Design: cohort study Participants: 1,708 Evidence: moderate

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

Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA neurology 2017-01-01

These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Self-rated health and its association with mortality in older adults in China, India and Latin America-a 10/66 Dementia Research Group study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Age and ageing 2017-11-01

However, in many low- and middle-income countries (LMIC) there is a lack of evaluation and the cross-cultural validity of SRH remains largely untested. 5 key findings →

Design: cohort study Participants: 16,940 Evidence: moderate

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

Age and diagnostic performance of Alzheimer disease CSF biomarkers

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2012-02-01

Core CSF changes in Alzheimer disease (AD) are decreased amyloid β(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively. 4 key findings →

Design: cross-sectional Participants: 529 Evidence: moderate

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

A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Acta neuropathologica 2019-05-27

The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →

Participants: 53,627 Evidence: low

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

Plasma proteins, cognitive decline, and 20-year risk of dementia in the Whitehall II and Atherosclerosis Risk in Communities studies

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-08-02

Plasma proteins affect biological processes and are common drug targets but their role in the development of Alzheimer's disease and related dementias remains unclear. 4 key findings →

Design: cohort study Evidence: moderate

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

Revised Diagnostic Criteria for Vascular Cognitive Impairment and Dementia—The VasCog-2-WSO Criteria

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA Neurology 2025-09-16

Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →

Participants: 49 Evidence: low

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

Clinical, imaging and blood biomarker outcomes in a Phase 3 clinical trial of tau aggregation inhibitor hydromethylthionine mesylate in mild cognitive impairment and mild to moderate dementia due to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. The Journal of Prevention of Alzheimer's Disease 2026-01-21

It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm. 5 key findings →

Design: phase-3-trial Participants: 598 Evidence: null result

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

CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios: better diagnostic markers of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Annals of clinical and translational neurology 2016-01-01

The CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios are significantly better than CSF Aβ42 to detect brain amyloid deposition in prodromal AD and to differentiate AD dementia from non-AD dementias. 5 key findings →

Participants: 1,182 Evidence: low

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

Plasma Biomarkers of Alzheimer Disease in Women With and Without HIV

✓ Peer-reviewed alzhub usefulness score 60 out of 100. JAMA network open 2023-11-01

These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV. 5 key findings →

Design: cohort study Participants: 307 Evidence: moderate

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

sTREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer's disease and associate with neuronal injury markers

✓ Peer-reviewed alzhub usefulness score 60 out of 100. EMBO molecular medicine 2016-05-02

TREM2 is an innate immune receptor expressed on the surface of microglia. 4 key findings →

Design: cross-sectional Evidence: low

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

Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Molecular neurodegeneration 2016-01-12

The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. 4 key findings →

Participants: 37 Evidence: moderate

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

Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer's disease pathology

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Nature aging 2022-11-28

The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) 1 . 4 key findings →

Design: longitudinal study Evidence: moderate

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

↑ Change the filters

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.

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
  • Randomized / 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
  • Multicenter 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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.

1,045 records (3.2% of the library) are not peer-reviewed — 966 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    Where this research is being discussed: events

Last updated