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Find studies

Showing 426–450 of 842 studies (page 18 of 34) · 27,380 in the whole library · How the 0–100 score works

Showing 842 studies tagged classification — clear

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.

TSPO and x c - overexpression can be assessed by [ 18 F]DPA-714 and [ 18 F]FSPG, respectively, and correlate with the level of Aβ plaque deposition obtained with a PET amyloid tracer. 5 key findings →

Design: longitudinal study Evidence: moderate

This software program with application of SPM8 plus DARTEL to VBM provides a high performance for AD diagnosis by using MRI. 1 key finding →

Participants: 45 Evidence: low

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

The results suggest that (11)C-PIB binding to Aβ deposits in transgenic mouse brain is highly dependent on the AD model and the structure of its Aβ plaques. 2 key findings →

Design: longitudinal study Evidence: moderate

Interest in understanding the roles of white matter (WM) inflammation and damage in the pathophysiology of Alzheimer disease (AD) has been growing significantly in recent years. 5 key findings →

Participants: 200 Evidence: low

Automated MRI-based classification of primary progressive aphasia variants

✓ Peer-reviewed alzhub usefulness score 49 out of 100. NeuroImage 2009-06-06

Degeneration of language regions in the dominant hemisphere can result in primary progressive aphasia (PPA), a clinical syndrome characterized by progressive deficits in speech and/or language function. 4 key findings →

Participants: 86 Evidence: low

The SVM can be used in single-subject discrimination and can help the clinician arrive at a diagnosis. 4 key findings →

Participants: 115 Evidence: low

The study of Alzheimer's disease (AD), the most common cause of dementia, faces challenges in terms of understanding the cause, monitoring the pathogenesis, and developing early diagnoses and effective treatments. 5 key findings →

Evidence: low

There is no disease-modifying treatment currently available for AD, one of the more impacting neurodegenerative diseases affecting more than 47.5 million people worldwide. 1 key finding →

Participants: 200 Evidence: moderate

Easily accessible biomarkers for Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal dementia (FTD), and related neurodegenerative disorders are urgently needed in an aging society to assist early-stage diagnoses. 4 key findings →

Participants: 377 Evidence: low

Magnetic resonance based volumetric measures of hippocampal formation, amygdala (A), caudate nucleus (CN), normalised for total intracranial volume (TIV), were analysed in relation to measures of cognitive deterioration and specific features of memory functions in 18 patients with probable Alzheimer's disease. 4 key findings →

Participants: 18 Evidence: low

Alzheimer's disease (AD) and frontotemporal dementia (FTD) are leading causes of cognitive decline. 4 key findings →

Design: cross-sectional Evidence: low

Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →

Evidence: low

The differential diagnosis of frontotemporal dementia (FTD) and Alzheimer's disease (AD) is difficult due to the overlaps of clinical symptoms. 4 key findings →

Participants: 47 Evidence: low

The subject groups for model derivation comprised 80 healthy subjects (HS), 36 patients with mild cognitive impairment (MCI) who converted to AD dementia within 18 months, 85 non-converter MCI patients who did not convert within 24 months, and 67 AD dementia patients with baseline FDG PET scan were recruited from the AD Neuroimaging Initiative (ADNI) database. 4 key findings →

Participants: 36 Evidence: moderate

The neurological deterioration associated with Alzheimer's disease (AD), involving accumulation of amyloid-beta peptides and neurofibrillary tangles, is associated with evident neuroinflammation. 4 key findings →

Evidence: moderate

Data from 17 107 individuals (321 Asian, 635 Black, 829 Hispanic, and 15 322 White) with MCI or dementia and amyloid PET were analyzed between April 2020 and January 2022. 5 key findings →

Design: cohort study Participants: 3,154 Evidence: moderate

This comprehensive review examines the integration of Quantitative Electroencephalography (qEEG) and Artificial Intelligence (AI) in the detection and diagnosis of Alzheimer's Disease (AD). 5 key findings →

Participants: 890 Evidence: low

Alzheimer’s disease (AD), a leading neurodegenerative disorder, progresses from an intermediary stage known as Mild Cognitive Impairment (MCI), characterized by measurable cognitive decline with retained functional independence. 1 key finding →

Design: longitudinal study Evidence: moderate

From across this tag

8 of the 838 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.

↑ Change the filters

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