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Find studies

Showing 26–50 of 79 studies with an author at Johns Hopkins Medicine (US) of type cohort or longitudinal study (page 2 of 4) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 79 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.

Late-life depression (LLD) is characterized by considerable heterogeneity in clinical manifestation. 4 key findings →

Design: longitudinal study Participants: 996 Evidence: moderate

Blood-Based Biomarkers and Risk of Onset of Mild Cognitive Impairment Over the Short and Long Term

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2024-12-26

This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →

Design: longitudinal study Participants: 271 Evidence: moderate

Stroke, dementia, and hypertension are associated with late-onset epilepsy; however, the role of other vascular and lifestyle factors remains unclear. 5 key findings →

Design: cohort study Participants: 792 Evidence: moderate

White matter hyperintensities and CSF Alzheimer disease biomarkers in preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2019-12-30

These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. 5 key findings →

Design: longitudinal study Participants: 274 Evidence: moderate

The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →

Design: longitudinal study Participants: 2,609 Evidence: moderate

Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. 4 key findings →

Design: longitudinal study Evidence: high

Risk Factors Associated With Late-Onset Epilepsy in Dementia and Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 65 out of 100. JAMA Neurology 2025-04-14

Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →

Design: longitudinal study Participants: 713 Evidence: moderate

= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →

Design: longitudinal study Participants: 6,471 Evidence: moderate

Growing evidence suggests that fine particulate matter (PM 2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. 5 key findings →

Design: cohort study Evidence: moderate

Plasma clusterin concentration is associated with longitudinal brain atrophy in mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 64 out of 100. NeuroImage 2011-07-28

Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). 5 key findings →

Design: longitudinal study Participants: 139 Evidence: moderate

This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →

Design: longitudinal study Participants: 273 Evidence: moderate

MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black. 5 key findings →

Design: longitudinal study Participants: 1,883 Evidence: moderate

Treatment with celecoxib or naproxen did not improve depressive symptoms over time compared with placebo. 5 key findings →

Design: longitudinal study Participants: 2,528 Evidence: high

Acceleration of Brain Atrophy and Progression From Normal Cognition to Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 63 out of 100. JAMA network open 2024-10-01

It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI). 4 key findings →

Design: cohort study Participants: 185 Evidence: moderate

Studies of long-term cognitive change should account for the potential effects of education on the outcome, since some studies have demonstrated an association of education with dementia risk. 4 key findings →

Design: cohort study Participants: 14,020 Evidence: moderate

Age at onset of Alzheimer's disease: relation to pattern of cognitive dysfunction and rate of decline

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurology 1994-07-01

We examined the pattern of cognitive impairment and rate of cognitive and functional decline as a function of age at symptom onset in 127 patients with probable Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Participants: 127 Evidence: moderate

Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →

Design: cohort study Participants: 37,096 Evidence: moderate

Understanding how dementia risk is impacted by timing of smoking cessation has public health implications for prevention efforts. 4 key findings →

Design: cohort study Participants: 1,347 Evidence: moderate

Dementia in AIDS patients: incidence and risk factors. Multicenter AIDS Cohort Study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 1993-11-01

We determined incidence and future projections of dementia after AIDS onset in 492 homosexual men with AIDS in the Baltimore/Los Angeles sites of the Multicenter AIDS Cohort Study, 64 of whom developed dementia. 3 key findings →

Design: cohort study Evidence: moderate

HIV-associated neurologic disease incidence changes:: Multicenter AIDS Cohort Study, 1990-1998

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2001-01-01

This study examined the temporal trends in the incidence rates of HIV dementia, cryptococcal meningitis, toxoplasmosis, progressive multifocal leukoencephalopathy, and CNS lymphoma from January 1990 to December 1998 in the Multicenter AIDS Cohort Study. 3 key findings →

Design: cohort study Evidence: moderate

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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
  • Randomized / 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
  • Multicenter 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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.

1,045 records (3.2% of the library) are not peer-reviewed — 966 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    Where this research is being discussed: events

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