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Research

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

Find studies

Showing 251–275 of 696 studies with an author at Mayo Clinic (US) (page 11 of 28) · 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

Authors

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

Other 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.

The Mayo Clinic Study of Aging: design and sampling, participation, baseline measures and sample characteristics

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuroepidemiology 2008-02-07

Strengths of the study are that the subjects were randomly selected from a defined population, the majority of the subjects were examined in person, and MCI was defined using published criteria. 1 key finding →

Participants: 2,719 Evidence: moderate

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

Detecting dementia with the mini-mental state examination in highly educated individuals

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Archives of neurology 2008-07-01

Older patients with a college education who present with complaints of cognitive decline (reported by themselves or others) and score less than 27 on the MMSE are at a greater risk of being diagnosed with dementia and should be referred for a comprehensive dementia evaluation, including formal neuropsychological testing. 2 key findings →

Participants: 307 Evidence: moderate

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

Antemortem MRI findings correlate with hippocampal neuropathology in typical aging and dementia

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neurology 2002-03-01

Individuals with an isolated pathologic diagnosis of AD, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle--only degeneration usually had substantial hippocampal atrophy, while those with changes of typical aging did not. 2 key findings →

Participants: 67 Evidence: low

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

TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2017-08-01

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features. 2 key findings →

Evidence: low

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

White matter hyperintensities: relationship to amyloid and tau burden

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Brain : a journal of neurology 2019-08-01

Although white matter hyperintensities have traditionally been viewed as a marker of vascular disease, recent pathology studies have found an association between white matter hyperintensities and Alzheimer's disease pathologies. 4 key findings →

Participants: 434 Evidence: low

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

Data-driven discovery of probable Alzheimer's disease and related dementia subphenotypes using electronic health records

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Learning health systems 2020-09-10

Four subphenotypes were computationally derived that correlated with cardiovascular diseases and mental health illnesses. 3 key findings →

Design: longitudinal study Participants: 273 Evidence: moderate

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

ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2022-03-16

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →

Evidence: low

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

Multi-organ distribution of phosphorylated alpha-synuclein histopathology in subjects with Lewy body disorders

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2010-03-21

A sensitive immunohistochemical method for phosphorylated alpha-synuclein was used to stain sets of sections of spinal cord and tissue from 41 different sites in the bodies of 92 subjects, including 23 normal elderly, 7 with incidental Lewy body disease (ILBD), 17 with Parkinson's disease (PD), 9 with dementia with Lewy bodies (DLB), 19 with Alzheimer's disease with Lewy bodies (ADLB) and 17 with Alzheimer's disease with no Lewy bodies (ADNLB). 5 key findings →

Participants: 92 Evidence: low

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

The inhibition of TDP-43 mitochondrial localization blocks its neuronal toxicity

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 2016-06-27

Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases. 5 key findings →

Evidence: low

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

Development of methodology for conducting clinical trials in frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Brain : a journal of neurology 2008-10-01

To design clinical trials for the frontotemporal lobar degenerations (FTLD), knowledge about measurement of disease progression is needed to estimate power and enable the choice of optimal outcome measures. 2 key findings →

Participants: 107 Evidence: low

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

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 1998-01-01

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. 4 key findings →

Evidence: low

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

Dual ontogeny of disease-associated microglia and disease inflammatory macrophages in aging and neurodegeneration

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Immunity 2022-08-04

Brain macrophage populations include parenchymal microglia, border-associated macrophages, and recruited monocyte-derived cells; together, they control brain development and homeostasis but are also implicated in aging pathogenesis and neurodegeneration. 4 key findings →

Evidence: low

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

Donanemab: Appropriate use recommendations

✓ Peer-reviewed alzhub usefulness score 58 out of 100. The journal of prevention of Alzheimer's disease 2025-03-27

Donanemab (Kisunla®), an IgG1 monoclonal antibody targeting N-terminal pyroglutamate-modified forms of amyloid-β, is approved in the United States for treatment of early symptomatic Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Comparison of plasma neurofilament light and total tau as neurodegeneration markers: associations with cognitive and neuroimaging outcomes

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Alzheimer's research & therapy 2021-12-14

Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →

Design: cross-sectional Participants: 995 Evidence: moderate

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

C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature neuroscience 2016-03-21

Neuronal inclusions of poly(GA), a protein unconventionally translated from G4C2 repeat expansions in C9ORF72, are abundant in patients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) caused by this mutation. 4 key findings →

Evidence: low

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

An FDG-PET–Based Machine Learning Framework to Support Neurologic Decision-Making in Alzheimer Disease and Related Disorders

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neurology 2025-06-27

The discovery cohort contained 3,671 individuals with a mean age of 68 years and consisted of 49% reported female. 5 key findings →

Participants: 3,671 Evidence: moderate

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

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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