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Find studies

Showing 401–425 of 432 studies with an author at Karolinska Institutet (SE) (page 17 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.

Inhibitors of the enzyme acetylcholinesterase (AChE) are presently used as long-term symptomatic treatments for patients with Alzheimer disease (AD), as they enhance central levels of synaptic acetylcholine. 4 key findings →

Evidence: low

In total, 24 recommendations were developed covering the research landscape and priorities within research in AD following a possible approval, potential impact on health care systems and diagnostic pathways, and communication to patients about anti-amyloid antibodies. 5 key findings →

Evidence: low

Higher education was associated with higher initial cognitive status but faster decline. 5 key findings →

Participants: 353 Evidence: low

Treatment strategies that are efficient against established Alzheimer's disease (AD) are needed. 2 key findings →

Evidence: low

There is evidence of geographical variation in dementia[1], not all of which can be ascribed to genetic factors[2]. 1 key finding →

Participants: 568 Evidence: low

We have successfully generated specific high affinity monoclonal antibodies against p -Tau217, p -Tau205, and N-terminus GFAP and have confirmed that these antibodies have the necessary specificity and sensitivity for the Simoa platform. 2 key findings →

Evidence: moderate

Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →

Evidence: low

Regional binding of tau and amyloid PET tracers in Down syndrome autopsy brain tissue

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular neurodegeneration 2020-11-23

This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD. 5 key findings →

Evidence: low

Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes. 3 key findings →

Evidence: low

Dynamic changes in PET amyloid and FDG imaging at different stages of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neurobiology of aging 2010-08-04

In this study 5 patients with mild cognitive impairment (MCI) and 9 Alzheimer's disease (AD) patients underwent respectively 3- and 5-year follow-up positron emission tomography (PET) studies with N-methyl [(11)C] 2-(4-methylaminophenyl)-6-hydroxy-benzothiazole ((11)C-PIB) and (18)F-fluorodeoxyglucose ((18)F-FDG) to understand the time courses in AD disease processes. 4 key findings →

Evidence: low

Three themes were identified: (1) Struggling with conflicting emotions and social challenges - caregivers reported experiencing stress, physical exhaustion, and emotional strain due to constant availability and the challenges of managing behavioral changes, further intensified by isolation and shrinking social networks. 5 key findings →

Evidence: low

Poststroke cognitive impairment (PSCI) refers to any level of cognitive decline occurring after a stroke, ranging from mild to severe impairments, while PSCI with dementia describes a more severe form where the cognitive decline significantly affects daily functioning and meets the clinical criteria for dementia. 2 key findings →

Evidence: low

Expert panels interpreted 1497 scans. Participants were a median age of 75 y (range, 65-96 y), 51.4% were female, and 60.5% had mild cognitive impairment. 5 key findings →

Evidence: low

Deregulation of amyloid precursor protein (APP) processing with increased production of amyloid beta-peptide (Abeta) is considered to be a key pathogenic event in Alzheimer's disease (AD). 4 key findings →

Design: clinical trial Evidence: low

Dementia poses an on-going Canadian challenge due to an aging population, with cases projected to rise significantly by 2050. 4 key findings →

Evidence: low

Individuals with dementia were more likely to have staff or family members present at death, to receive documented decisions to shift to EOL care, have symptom assessments made the final week of life and prescription of injectables. 5 key findings →

Participants: 39 Evidence: low

Decreased cyclin dependent kinase in brain of patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Neuroscience letters 1996-09-01

In order to study whether phosphokinases might be involved in the neuropathology of Down Syndrome (DS) and Alzheimer disease (AD), cyclin dependent kinase (CDK) activity and protein, phosphokinase C (PKC) and phosphokinase A (PKA) activities have been determined in frontal lobes of DS, AD and control brains. 1 key finding →

Evidence: low

Early diagnosis of Alzheimer disease with positron emission tomography

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Alzheimer disease and associated disorders 2000-01-01

The emergence of drugs that may slow progression of Alzheimer disease, if administered early during its course, has necessitated early diagnosis of the disease itself. 3 key findings →

Evidence: low

Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →

Evidence: low

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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 →

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