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Research

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

Find studies

Showing 1–24 of 24 studies by Toledo JB with an author at University of Pennsylvania (US) · 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

Other 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.

Predicting clinical decline and conversion to Alzheimer's disease or dementia using novel Elecsys Aβ(1-42), pTau and tTau CSF immunoassays

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Scientific reports 2019-12-13

We evaluated the performance of CSF biomarkers for predicting risk of clinical decline and conversion to dementia in non-demented patients with cognitive symptoms. 4 key findings →

Design: longitudinal study Participants: 619 Evidence: moderate

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

Neuropathological consensus criteria for the evaluation of Lewy pathology in post-mortem brains: a multi-centre study

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Acta neuropathologica 2021-01-05

The category of neocortical LP according to the LPC system was associated with a 5.9 OR (p < 0.0001) of dementia in the 134 NBTR cases and a 3.14 OR (p = 0.0001) in the 202 UPBB cases. 2 key findings →

Participants: 202 Evidence: low

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

Heterogeneity of neuroanatomical patterns in prodromal Alzheimer's disease: links to cognition, progression and biomarkers

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Brain : a journal of neurology 2017-03-01

See Coulthard and Knight (doi:10.1093/aww335) for a scientific commentary on this article. 1 key finding →

Design: longitudinal study Participants: 530 Evidence: moderate

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

White matter lesions: Spatial heterogeneity, links to risk factors, cognition, genetics, and atrophy

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Neurology 2018-08-03

These results support the hypothesis that the appearance of WMH follows age and disease-dependent regional distribution patterns, potentially influenced by differential underlying pathophysiologic mechanisms, and possibly with a differential link to vascular and neurodegenerative changes. 5 key findings →

Design: cross-sectional Participants: 1,836 Evidence: moderate

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

Nonlinear Association Between Cerebrospinal Fluid and Florbetapir F-18 β-Amyloid Measures Across the Spectrum of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA neurology 2015-05-01

The association between both biomarkers is limited to a middle range of values, is modified by the APOE genotype, and is absent for longitudinal changes; 4 different approaches in 2 different platforms converge on similar pathological Aβ cutoff levels; and different pipelines to process PET scans showed correlated but not identical results. 5 key findings →

Design: cohort study Participants: 820 Evidence: moderate

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

CSF α-synuclein improves diagnostic and prognostic performance of CSF tau and Aβ in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Acta neuropathologica 2013-06-29

Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments. 4 key findings →

Design: longitudinal study Participants: 389 Evidence: moderate

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

Contribution of cerebrovascular disease in autopsy confirmed neurodegenerative disease cases in the National Alzheimer's Coordinating Centre

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Brain : a journal of neurology 2013-07-10

Cerebrovascular disease and vascular risk factors are associated with Alzheimer's disease, but the evidence for their association with other neurodegenerative disorders is limited. 3 key findings →

Evidence: low

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

Advanced brain aging: relationship with epidemiologic and genetic risk factors, and overlap with Alzheimer disease atrophy patterns

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Translational psychiatry 2016-04-05

We systematically compared structural imaging patterns of advanced brain aging (ABA) in the general-population, herein defined as significant deviation from typical BA to those found in Alzheimer disease (AD). 5 key findings →

Participants: 2,705 Evidence: moderate

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

Sequential distribution of pTDP-43 pathology in behavioral variant frontotemporal dementia (bvFTD)

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Acta neuropathologica 2014-01-10

We examined regional distribution patterns of phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) intraneuronal inclusions in frontotemporal lobar degeneration (FTLD). 1 key finding →

Participants: 39 Evidence: low

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

Longitudinal change in CSF Tau and Aβ biomarkers for up to 48 months in ADNI

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2013-06-29

The dynamics of cerebrospinal fluid (CSF) tau and Aβ biomarkers over time in Alzheimer's disease (AD) patients from prodromal pre-symptomatic to severe stages of dementia have not been clearly defined and recent studies, most of which are cross-sectional, present conflicting findings. 4 key findings →

Design: cross-sectional Evidence: moderate

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

Memory, executive, and multidomain subtle cognitive impairment: clinical and biomarker findings

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 2015-06-17

We studied the biomarker signatures and prognoses of 3 different subtle cognitive impairment (SCI) groups (executive, memory, and multidomain) as well as the subjective memory complaints (SMC) group. 4 key findings →

Participants: 522 Evidence: low

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

Cerebrospinal fluid α-synuclein contributes to the differential diagnosis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2018-03-28

The ability of Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers (amyloid β peptide 1-42, total tau, and phosphorylated tau) to discriminate AD from related disorders is limited. 4 key findings →

Participants: 367 Evidence: low

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

Integration and relative value of biomarkers for prediction of MCI to AD progression: spatial patterns of brain atrophy, cognitive scores, APOE genotype and CSF biomarkers

✓ Peer-reviewed alzhub usefulness score 50 out of 100. NeuroImage. Clinical 2013-11-28

This study evaluates the individual, as well as relative and joint value of indices obtained from magnetic resonance imaging (MRI) patterns of brain atrophy (quantified by the SPARE-AD index), cerebrospinal fluid (CSF) biomarkers, APOE genotype, and cognitive performance (ADAS-Cog) in progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) within a variable follow-up period up to 6 years, using data from the Alzheimer's Disease Neuroimaging Initiative-1 (ADNI-1). 4 key findings →

Evidence: low

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

Microglial activation and TDP-43 pathology correlate with executive dysfunction in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2012-01-01

While cognitive deficits are increasingly recognized as common symptoms in amyotrophic lateral sclerosis (ALS), the underlying histopathologic basis for this is not known, nor has the relevance of neuroinflammatory mechanisms and microglial activation to cognitive impairment (CI) in ALS been systematically analyzed. 4 key findings →

Evidence: low

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

Comparison of cerebrospinal fluid levels of tau and Aβ 1-42 in Alzheimer disease and frontotemporal degeneration using 2 analytical platforms

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Archives of neurology 2012-08-01

Cerebrospinal fluid values of total tau (T-tau) and β-amyloid 1-42 (Aβ 1-42) obtained using the Innotest enzyme-linked immunosorbent assay were transformed using a linear regression model to equivalent values obtained using the INNO-BIA AlzBio3 (xMAP; Luminex) assay. 4 key findings →

Evidence: low

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

Can MRI screen for CSF biomarkers in neurodegenerative disease?

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurology 2012-12-26

Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) may have overlapping clinical presentations despite distinct underlying neuropathologies, thus making in vivo diagnosis challenging. 4 key findings →

Participants: 185 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 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