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Find studies

Showing 76–100 of 116 studies with an author at University of Rochester Medicine (US) (page 4 of 5) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 116 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.

SNF discharges decreased while home and HHA discharges increased during the pandemic. 5 key findings →

Participants: 830,656 Evidence: moderate

In vivo amyloid imaging in autopsy-confirmed Parkinson disease with dementia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neurology 2010-01-01

[(11)C]-Pittsburgh Compound B (PIB) PET is specific for fibrillar Abeta molecular pathology but not for pathologic diagnosis of comorbid Alzheimer disease in individuals with Parkinson disease dementia. 1 key finding →

Evidence: low

Targeting innate immunity for neurodegenerative disorders of the central nervous system

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurochemistry 2016-09-01

Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. 4 key findings →

Evidence: low

Neuroinflammation is a conspicuous feature of Alzheimer disease (AD) pathology and is thought to contribute to the ultimate neurodegeneration that ensues. 4 key findings →

Evidence: low

Microinfarcts occur commonly in the aging brain as a consequence of diffuse embolic events and are associated with the development of vascular dementia and Alzheimer's disease. 4 key findings →

Evidence: low

Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. 4 key findings →

Evidence: low

Accumulation of amyloid beta-peptide (Abeta) in the central nervous system (CNS) may initiate pathogenic cascades mediating neurovascular and neuronal dysfunctions associated with the development of cerebral beta-amyloidosis and cognitive decline in patients with Alzheimer disease (AD) and with related familial cerebrovascular disorders. 3 key findings →

Evidence: low

Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes. 4 key findings →

Evidence: low

Microinfarcts are a common clinical feature of the aging brain, particularly in patients with cognitive decline or vascular or Alzheimer's dementia. 4 key findings →

Evidence: low

We examined state variations in assisted living (AL) regulatory policies for admission/retention, staffing/training, medication management, and dementia care. 3 key findings →

Participants: 46 Evidence: low

Role of the blood-brain barrier in the pathogenesis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Current Alzheimer research 2007-04-01

Cerebrovascular dysfunction contributes to the cognitive decline and dementia in Alzheimer's disease (AD), and may precede cerebral amyloid angiopathy and brain accumulation of the Alzheimer's neurotoxin, amyloid beta-peptide (Abeta). 4 key findings →

Evidence: low

In China, the crude mortality from AD and other forms of dementia increased from 2009 to 2015, but the age-standardized mortality decreased. 5 key findings →

Evidence: low

A significant correlation was found between perceived cognitive decline and increased motivation to engage in dementia risk reduction behaviors (r = 0.44). 4 key findings →

Design: cross-sectional Evidence: low

Gridlock in hospital medicine

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of Hospital Medicine 2023-12-12

Before the COVID-19 pandemic, supply and demand forcast models predicted significant nursing shortages across the United States through 2030 due to both an aging patient population and nursing workforce.1, 2 However, during the pandemic, we saw an exodus of younger nurses in addition to early retirements. 5 key findings →

Participants: 100 Evidence: low

Key independent variables included the interaction of NH quality (measured by 5‐star rating) and race (i.e. black versus white), and interaction of NH quality, race, and state Medicaid dementia‐related add‐on policies. 4 key findings →

Participants: 874,526 Evidence: low

Exploring the unmet needs of Latino dementia caregivers: a qualitative study

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Gerontologist 2025-09-09

Four themes were derived from the data analysis as key areas of caregiving needs for Latinos: need to connect socially with others; need for resources to provide care; need to understand dementia and navigating existing resources and future care planning; and need for empathic, culturally congruent healthcare. 3 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 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