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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 201–225 of 337 studies with an author at Mayo Clinic in Florida (US) (page 9 of 14) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 337 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; 13,658 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.

Genome-wide association study of neuropathological features in Lewy body disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Brain 2025-03-14

APOE ε4) was associated with a greater severity of each of Braak NFT stage [odds ratio (OR) = 3.07, P = 2.34 × 10-32], Thal amyloid phase (OR = 3.57, P = 3.28 × 10-29) and LBD subtype (OR = 1.78, P = 9.85 × 10-9), with similar findings observed in the independent replication series (Braak NFT stage, OR = 2.30, P = 2.70 × 10-11; Thal amyloid phase, OR = 3.17, P = 6.39 × 10-18; LBD subtype, OR = 2.68, P = 3.85 × 10-10). 5 key findings →

Participants: 980 Evidence: low

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

Neuropathology and molecular diagnosis of Synucleinopathies

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular neurodegeneration 2021-12-18

Synucleinopathies are clinically and pathologically heterogeneous disorders characterized by pathologic aggregates of α-synuclein in neurons and glia, in the form of Lewy bodies, Lewy neurites, neuronal cytoplasmic inclusions, and glial cytoplasmic inclusions. 2 key findings →

Evidence: low

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

Age-dependent neurofibrillary tangle formation, neuron loss, and memory impairment in a mouse model of human tauopathy (P301L)

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2005-11-01

Here, we describe the generation of a novel transgenic mouse model of human tauopathy. 5 key findings →

Evidence: low

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

The role of tau in neurodegeneration

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular neurodegeneration 2009-03-11

Since the identification of tau as the main component of neurofibrillary tangles in Alzheimer's disease and related tauopathies, and the discovery that mutations in the tau gene cause frontotemporal dementia, much effort has been directed towards determining how the aggregation of tau into fibrillar inclusions causes neuronal death. 1 key finding →

Evidence: low

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

TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-01-11

Triggering Receptor Expressed on Myeloid cells 2 (TREM2), which is expressed on myeloid cells including microglia in the CNS, has recently been identified as a risk factor for Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Cerebrospinal fluid inflammatory markers in Parkinson's disease--associations with depression, fatigue, and cognitive impairment

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Brain, behavior, and immunity 2013-07-31

Neuroinflammation may be involved in the pathophysiology of Parkinson's disease (PD) and specifically in non-motor symptoms such as depression, fatigue and cognitive impairment. 4 key findings →

Participants: 87 Evidence: low

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

Molecular features of human pathological tau distinguish tauopathy-associated dementias

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cell 2026-01-29

In Alzheimer's disease (AD), pathological tau protein shows a progressive accumulation of post-translational modifications (PTMs), reflecting disease severity, progression, and prion-like activity. 5 key findings →

Evidence: low

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

Sex differences in clinical phenotypes of behavioral variant frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Alzheimer s & Dementia 2025-04-01

Females with sporadic bvFTD showed worse compulsive behavior (p = 0.026) and language impairments (p = 0.024) compared to females with genetic bvFTD (n = 152). 5 key findings →

Participants: 152 Evidence: low

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

Location of pathogenic variants in PSEN1 impacts progression of cognitive, clinical, and neurodegenerative measures in autosomal-dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Aging cell 2023-06-08

Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →

Design: cross-sectional Evidence: moderate

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

Machine Learning Models of Polygenic Risk for Enhanced Prediction of Alzheimer Disease Endophenotypes

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology. Genetics 2024-01-10

We found that ML-PRS approaches improved upon standard PRS for prediction of AD endophenotypes, partly related to improved accounting for nonlinear effects of genetic susceptibility alleles. 3 key findings →

Participants: 1,791 Evidence: low

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

Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Cold Spring Harbor perspectives in medicine 2012-03-01

Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective. 5 key findings →

Evidence: low

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

Suspected non-Alzheimer disease pathophysiology--concept and controversy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature reviews. Neurology 2016-01-18

Suspected non-Alzheimer disease pathophysiology (SNAP) is a biomarker-based concept that applies to individuals with normal levels of amyloid-β biomarkers in the brain, but in whom biomarkers of neurodegeneration are abnormal. 1 key finding →

Evidence: low

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

Cognitive domain decline in healthy apolipoprotein E epsilon4 homozygotes before the diagnosis of mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Archives of neurology 2007-09-01

Of 214 participants, 48 showed no decline on any test, 126 showed decline on only 1 test in 1 or more domains, and 40 showed decline on 2 or more tests in 1 or more domains. 2 key findings →

Participants: 214 Evidence: low

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

Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2015-09-15

Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →

Evidence: moderate

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

C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science translational medicine 2020-09-01

TAR DNA-binding protein 43 (TDP-43) inclusions are a pathological hallmark of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), including cases caused by G 4 C 2 repeat expansions in the C9orf72 gene (c9FTD/ALS). 3 key findings →

Evidence: low

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

Neuropathology of variants of progressive supranuclear palsy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Current opinion in neurology 2010-08-01

Neurodegenerative tauopathies, of which progressive supranuclear palsy (PSP) is one of the most common, are clinically heterogeneous, reflecting differences in distribution and biochemical composition of tau pathology. 1 key finding →

Evidence: low

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

Neuropathologically defined subtypes of Alzheimer's disease differ significantly from neurofibrillary tangle-predominant dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2012-09-12

Alzheimer's disease (AD) can be classified based on the relative density of neurofibrillary tangles (NFTs) in the hippocampus and association cortices into three subtypes: typical AD, hippocampal-sparing AD (HpSp AD), and limbic-predominant AD (LP AD). 4 key findings →

Participants: 18 Evidence: low

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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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