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Find studies

Showing 76–100 of 432 studies with an author at Karolinska Institutet (SE) (page 4 of 18) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 432 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.

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.

Parkinson's disease has a long prodromal stage with various subclinical motor and non-motor manifestations; however, their evolution in the years before Parkinson's disease is diagnosed is unclear. 5 key findings →

Design: longitudinal study Evidence: moderate

The mean age was 70.9 years (standard deviation, 5.9), 57.2% were women, 40.6% were illiterate, and 88.3% were farmers. 2 key findings →

Participants: 5,765 Evidence: high

Patterns of chronic multimorbidity in the elderly population

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Journal of the American Geriatrics Society 2009-02-01

In persons with multimorbidity, there exists co-occurrence of diseases beyond chance, which clinicians need to take into account in their daily practice. 2 key findings →

Design: prospective cohort Participants: 1,099 Evidence: moderate

Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 1998-06-01

Thirteen families have been described with an autosomal dominantly inherited dementia named frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), historically termed Pick's disease. 5 key findings →

Evidence: low

These results demonstrate an important role of clusterin in the pathogenesis of AD and suggest that alterations in amyloid chaperone proteins may be a biologically relevant peripheral signature of AD. 4 key findings →

Design: longitudinal study Evidence: moderate

The trajectories of core Alzheimer disease (AD) cerebrospinal fluid (CSF) biomarkers and the concurrent cognitive changes across the clinical spectrum remain unclear yet are important for clinical trial design. 4 key findings →

Design: cohort study Participants: 197 Evidence: moderate

One million nine hundred twenty-five thousand, five hundred sixty-three individuals were included across the four databases with a median follow-up ranging from 5.6 to 8.4 years. 4 key findings →

Design: meta-analysis Evidence: high

This study highlights challenges for the reproducibility of α-syn SAA results across different protocols applied by different laboratories. 5 key findings →

Design: cross-sectional Participants: 30 Evidence: early

Mean annual costs for individuals with clinically diagnosed AD were SEK 99,906, SEK 290,972, SEK 479,524, and SEK 795,617 in mild cognitive impairment (MCI), mild, moderate, and severe AD. 1 key finding →

Design: cohort Participants: 95,853 Evidence: high

Polygenic Overlap Between C-Reactive Protein, Plasma Lipids, and Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Circulation 2015-04-10

By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →

Evidence: low

Evidence strongly supports the important role of insulin resistance in cognitive decline and dementia and suggests that insulin sensitizers may protect against cognitive decline in diabetic and pre-diabetic individuals. 5 key findings →

Design: cross-sectional Participants: 204 Evidence: moderate

ATN (β-amyloid [Aβ], tau, neurodegeneration) system categorizes individuals based on their core Alzheimer disease (AD) biomarkers. 4 key findings →

Design: cross-sectional Participants: 410 Evidence: low

Disease-modifying effects of TMEM106B in genetic frontotemporal dementia: a longitudinal GENFI study

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Brain 2025-04-22

Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →

Design: cohort study Participants: 518 Evidence: moderate

Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Annals of Neurology 2004-01-21

This report describes the first human study of a novel amyloid-imaging positron emission tomography (PET) tracer, termed Pittsburgh Compound-B (PIB), in 16 patients with diagnosed mild AD and 9 controls. 3 key findings →

Participants: 16 Evidence: low

In addition to the deposition of β-amyloid plaques, neurofibrillary tangles composed of aggregated hyperphosphorylated tau are one of the pathological hallmarks of Alzheimer's disease and other neurodegenerative disorders. 1 key finding →

Design: systematic review Evidence: high

Influence of social network on occurrence of dementia: a community-based longitudinal study

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Lancet (London, England) 2000-04-01

Those individuals living alone, and those without any close social ties, both had an adjusted relative risk for developing dementia of 1.5 (95% CI 1.0-2.1 and 1.0-2.4, respectively). 2 key findings →

Participants: 176 Evidence: moderate

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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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