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Find studies

Showing 101–125 of 264 studies with an author at Rush University Medical Center (US) (page 5 of 11) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 264 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.

Cognitive function was inversely related to all measures of disease pathology, indicating lower function at more severe levels of pathology. 2 key findings →

Design: longitudinal study Evidence: moderate

New technology is convenient for measuring blood total tau concentrations and provides a unique and increased opportunity for early intervention to slow cognitive decline. 4 key findings →

Design: cohort study Participants: 1,159 Evidence: moderate

For one of the primary analyses, the interpretation of the florbetapir scans (majority interpretation of five nuclear medicine physicians, who classified each scan as amyloid positive or amyloid negative) was compared with amyloid pathology (assessed according to the Consortium to Establish a Registry for Alzheimer's Disease standards, and classed as amyloid positive for moderate or frequent plaques or amyloid negative for no or sparse plaques); correlation of the image analysis results with amyloid burden was tested as a coprimary endpoint. 3 key findings →

Participants: 59 Evidence: low

Vascular burden and Alzheimer disease pathologic progression

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurology 2012-09-12

Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →

Design: longitudinal study Evidence: moderate

MIND Dietary Pattern and Its Association with Cognition and Incident Dementia in the UK Biobank

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Nutrients 2022-12-21

A high adherence to the Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurodegenerative Delay (MIND) has been associated with better cognition and a lower risk of dementia in some but not all studies. 4 key findings →

Participants: 120,661 Evidence: low

MIND Diet and Hippocampal Sclerosis Among Community-Based Older Adults

✓ Peer-reviewed alzhub usefulness score 60 out of 100. JAMA Network Open 2025-08-07

Among 809 participants (mean [SD] age at death, 91.3 [6.1] years; 538 [72%] female; mean [SD] follow-up, 7.2 [4.4] years), HS was present in 82 (10.1%) participants; 71 participants (9%) had both HS and LATE-NC, and in the scored subset, 43 participants (14%) had moderate and 35 participants (12%) had severe hippocampal neuronal loss. 5 key findings →

Design: cohort study Participants: 300 Evidence: moderate

Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →

Design: cohort Participants: 8,582 Evidence: high

Cardiovascular Health and Biomarkers of Neurodegenerative Disease in Older Adults

✓ Peer-reviewed alzhub usefulness score 59 out of 100. JAMA network open 2025-03-03

These findings suggest that promoting CVH in older adults may help alleviate the burden of neurodegenerative diseases, particularly among Black adults, who are known to experience a higher prevalence of cardiovascular disease. 5 key findings →

Design: cohort study Participants: 1,018 Evidence: moderate

Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. 3 key findings →

Evidence: low

The neuropathology of probable Alzheimer disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Annals of neurology 2009-08-01

Of 179 persons (average age, 86.9 years) with probable AD, 87.7% had pathologically confirmed AD, and 45.8% had mixed pathologies, most commonly AD with macroscopic infarcts (n = 54), followed by AD with neocortical LB disease (n = 19) and both (n = 8). 1 key finding →

Participants: 54 Evidence: low

TAR DNA-binding protein 43 (TDP-43) is a major pathological protein of sporadic and familial frontotemporal lobar degeneration with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). 1 key finding →

Participants: 36 Evidence: low

Integrated Systems Approach Identifies Genetic Nodes and Networks in Late-Onset Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Cell 2013-04-01

The study constructed gene-regulatory networks in postmortem brain tissues from late-onset Alzheimer's disease patients and nondemented subjects to characterize associated molecular systems. 3 key findings →

The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →

Design: cohort study Participants: 624 Evidence: moderate

Mild cognitive impairment is common in nondemented Parkinson's disease (PD) patients and may be a harbinger of dementia. 1 key finding →

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 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