The concept of cognitive impairment intervening between normal ageing and very early dementia has been in the literature for many years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The concept of cognitive impairment intervening between normal ageing and very early dementia has been in the literature for many years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Magnetic resonance imaging (MRI)-based volumetric measurements of medial temporal lobe (MTL) structures can discriminate between normal elderly control subjects and patients with Alzheimer's disease (AD) of moderate to advanced severity. 1 key finding →
Participants: 94 Evidence: low
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Our data suggest that [F-18]-AV-1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1451 off-target binding. 3 key findings →
Evidence: low
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Alzheimer's disease affects millions of people around the world. 1 key finding →
Evidence: low
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Alzheimer's disease is a progressive, irreversible neurodegenerative disease impacting cognition, function, and behavior. 5 key findings →
Evidence: low
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The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD). 5 key findings →
Evidence: low
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Niney-two PD patients developed dementia, and 48 remained cognitively normal. 2 key findings →
Evidence: low
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Hippocampal atrophy is not specific for AD but is also seen in semantic dementia. 2 key findings →
Participants: 26 Evidence: low
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Frontotemporal lobar degeneration (FTLD) is the umbrella term encompassing a heterogeneous group of pathological disorders. 5 key findings →
Evidence: low
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CBD was associated with 4 clinical syndromes: progressive nonfluent aphasia (n = 5), behavioral variant frontotemporal dementia (n = 5), executive-motor (n = 7), and posterior cortical atrophy (n = 1). 2 key findings →
Participants: 18 Evidence: low
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Our results show that TREM2 is responsible for an unexpectedly high number of dementia cases in our cohort, suggesting that this gene should be taken into account when mutations in other dementia genes are excluded. 4 key findings →
Evidence: moderate
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Using DSM-IV criteria, 55 of 280 patients (19.6%) had delirium versus 17.6% using the CAM. 1 key finding →
Participants: 280 Evidence: low
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Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV-1451 binding and suggests complexity in AV-1451 binding. 4 key findings →
Participants: 38 Evidence: low
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In neurodegeneration research, normalization of regional volumes by intracranial volume (ICV) is important to estimate the extent of disease-driven atrophy. 1 key finding →
Participants: 406 Evidence: moderate
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The frontal lobes are most severely affected by SIVD. 4 key findings →
Participants: 78 Evidence: low
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During follow-up, 13 healthy patients converted to MCI or Alzheimer disease (AD), whereas 39 MCI subjects converted to AD. 5 key findings →
Participants: 72 Evidence: low
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18 F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. 3 key findings →
Participants: 33 Evidence: low
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Parietal and occipital lobar CMBs counts were higher in PiB(+) ADCI with moderate WMH than PiB(+) ADCI with minimal WMH, whereas PiB(-) patients with SVCI (ie, "pure" SVCI) showed both lobar and deep CMBs. 3 key findings →
Participants: 226 Evidence: moderate
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These findings suggest that CSF VILIP-1 and VILIP-1/Aβ42 offer diagnostic utility for early AD, and can predict future cognitive impairment in cognitively normal individuals similarly to tau and tau/Aβ42, respectively. 3 key findings →
Participants: 211 Evidence: moderate
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Biomarkers for Alzheimer's disease (AD) based on non-invasive methods are highly desirable for diagnosis, disease progression, and monitoring therapeutics. 4 key findings →
Design: longitudinal study Evidence: moderate
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In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →
Design: longitudinal study Evidence: moderate
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Age is the strongest risk factor for sporadic Alzheimer disease (AD), yet the effects of age on rates of clinical decline and brain atrophy in AD have been largely unexplored. 2 key findings →
Design: longitudinal study Participants: 723 Evidence: moderate
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Subjective cognitive failures (SCF) are associated with lower hippocampal volume, even in subjects without objective cognitive impairment and independent of white matter lesions. 2 key findings →
Design: cohort study Participants: 503 Evidence: moderate
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Senile plaques are a prominent pathological feature of Alzheimer's disease (AD), but little is understood about the association of glial cells with plaques or about the dynamics of glial responses through the disease course. 2 key findings →
Participants: 91 Evidence: low
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Unlike professional caregivers such as physicians and nurses, informal caregivers, typically family members or friends, provide care to individuals with a variety of conditions including advanced age, dementia, and cancer. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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.
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.
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 →