Participants: 108 Evidence: low
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28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Participants: 108 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The ACE is a brief and reliable bedside instrument for early detection of dementia, and offers a simple objective index to differentiate AD and FTD in mildly demented patients. 2 key findings →
Participants: 115 Evidence: low
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Reliability of the ACE-R was very good (alpha coefficient=0.8). 2 key findings →
Participants: 241 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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FTD is a malignant disorder with limited life expectancy. 5 key findings →
Participants: 31 Evidence: low
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We have previously reported a large Danish pedigree with autosomal dominant frontotemporal dementia (FTD) linked to chromosome 3 (FTD3). 2 key findings →
Evidence: low
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The cortical anatomy of 6 patients with semantic dementia (the temporal lobe variant of frontotemporal dementia) was contrasted with that of a group of age-matched normal subjects by using voxel-based morphometry, a technique that identifies changes in gray matter volume on a voxel-by-voxel basis. 4 key findings →
Evidence: low
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Over the past decade it has become evident that a substantial minority of patients with primary dementing diseases, particularly those presenting in the presenium, have dementia of frontal lobe type (DFT) due to non-Alzheimer's pathology. 1 key finding →
Design: longitudinal study Participants: 52 Evidence: moderate
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The double dissociation in performance on semantic memory and attention/executive function clearly separated the temporal and frontal variants of FTD and aids the early differentiation of FTD from AD. 3 key findings →
Evidence: low
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Change in eating behaviour was significantly more common in both of the frontotemporal dementia groups than in Alzheimer's disease. 2 key findings →
Participants: 23 Evidence: low
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The speech of patients with progressive non-fluent aphasia (PNFA) has often been described clinically, but these descriptions lack support from quantitative data. 1 key finding →
Participants: 15 Evidence: low
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Disturbed sleep cycles are the principal cause of institutionalization in dementia, and therefore represent a major clinical problem. 5 key findings →
Design: cross-sectional Evidence: moderate
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The development of novel treatments for Alzheimer's disease (AD), aimed at ameliorating symptoms and modifying disease processes, increases the need for early diagnosis. 1 key finding →
Participants: 26 Evidence: low
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Progressive non-fluent aphasia (PNFA) is a syndrome in which patients lose the ability to communicate fluently in the context of relative preservation of single word comprehension and non-linguistic cognitive abilities. 4 key findings →
Evidence: low
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Two patients with nonfluent progressive aphasia, who have been studied longitudinally, are contrasted with a group of 5 patients with fluent progressive aphasia or semantic dementia. 5 key findings →
Evidence: low
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Contrary to some prior reports, behavioral variant frontotemporal dementia (bv-FTD) patients who progress over time are typically impaired on executive tasks at first presentation, although an important minority of true FTD patients perform normally. 3 key findings →
Evidence: low
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We demonstrate that phonological and articulatory impairments may occur at presentation or early in the course of Alzheimer's disease, contrary to claims that these aspects of language production are relatively preserved until the final stages of this disease. 1 key finding →
Evidence: low
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Progressive and non-progressive patients are difficult to differentiate on the basis of current clinical diagnostic criteria for FTD but a combination of general cognitive, executive dysfunction and impaired ADL measures appear to be the most promising discriminators. 2 key findings →
Participants: 71 Evidence: low
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The presence of cognitive impairment in corticobasal degeneration (CBD) is now widely recognised. 1 key finding →
Evidence: low
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Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam. 2 key findings →
Evidence: low
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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
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →