27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Different duplications of the APP locus have been identified in five families with autosomal dominant early onset Alzheimer's disease (ADEOAD) and Abeta-related cerebral amyloid angiopathy (CAA). 4 key findings →
Participants: 21 Evidence: low
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To what degree does the so-called 'initial hit' of the brain versus chronic epilepsy contribute towards the memory impairment observed in chronic temporal lobe epilepsy (TLE) patients? 4 key findings →
Design: cross-sectional Participants: 1,156 Evidence: low
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Mid-life stroke risk factors have been related to late-life cognitive impairment. 4 key findings →
Participants: 1,841 Evidence: moderate
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Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →
Participants: 1,524 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From clinically based series it has been proposed that, in homozygotes for the apolipoprotein E epsilon 4 (apoE epsilon 4) allele, Alzheimer's disease is almost inevitable by the age of 80. 4 key findings →
Participants: 638 Evidence: low
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Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. 4 key findings →
Participants: 51 Evidence: low
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The study included 356,173 participants (median age 56 years; 53.69% female). 5 key findings →
Participants: 356,173 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated whether a discrepancy between chronological and biological age in midlife and late-life is associated with cognition and dementia risk. 5 key findings →
Design: cohort study Participants: 11,758 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD. 4 key findings →
Design: longitudinal study Evidence: moderate
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The distribution and density of neurofibrillary tangles and amyloid plaques was studied in a unique series of cases whose premortem cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very mildly demented cases (CDR = 0.5), and 8 severely demented (CDR = 3) cases. 5 key findings →
Evidence: low
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Compared to CTR, both AD-αSAA- and AD-αSAA+ showed widespread cortical thinning. 3 key findings →
Participants: 139 Evidence: low
Full summary, score breakdown and related studies → Original source
The clinical heterogeneity of multiple system atrophy (MSA) may, along with the primary aggregation of alpha-synuclein (α-syn), partly be shaped by co-pathologies, such as amyloid-beta (Aβ), phosphorylated (p)-tau, and pTDP-43, though their relevance remains unclear. 3 key findings →
Participants: 70 Evidence: moderate
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Of 1352 participants, 502 (37%) had LATE-NC (23% stage 1a, 6% stage 1b, 58% stage 2, 13% stage 3). 5 key findings →
Participants: 1,352 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared with healthy controls, patients with ALS - particularly those with cognitive impairment (ALSci) or ALS-FTD - showed elevated AD-related biomarkers. 5 key findings →
Participants: 192 Evidence: low
Full summary, score breakdown and related studies → Original source
Among CAA participants, 29 met CSF criteria for AD co-pathology. 4 key findings →
Participants: 231 Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is the second most common neurodegenerative cause of dementia, behind Alzheimer's disease (AD). 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The levels of α-synuclein oligomers and oligomers/total-α-synuclein ratio in CSF were higher in the PD group (n = 32; p < 0.0001, Mann-Whitney U test) compared to the control group (n = 28). 5 key findings →
Design: cross-sectional Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of toxic protein aggregates-amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles-is the pathological hallmark of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Neuropsychiatric symptoms (NPS) are core features of Alzheimer's disease and related dementias. 3 key findings →
Evidence: low
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Fluorodeoxyglucose positron emission tomography (PET) studies have found that patients with Alzheimer's dementia (AD) have abnormally low rates of cerebral glucose metabolism in posterior cingulate, parietal, temporal, and prefrontal cortex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
An (18)F-labeled PET amyloid-beta (Abeta) imaging agent could facilitate the clinical evaluation of late-life cognitive impairment by providing an objective measure for Alzheimer disease (AD) pathology. 4 key findings →
Design: open-label trial Participants: 16 Evidence: low
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Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. 4 key findings →
Evidence: low
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Cortical superficial siderosis describes a distinct pattern of blood-breakdown product deposition limited to cortical sulci over the convexities of the cerebral hemispheres, sparing the brainstem, cerebellum and spinal cord. 4 key findings →
Evidence: low
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Amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) constitutes a devastating disease spectrum characterized by 43-kDa TAR DNA-binding protein (TDP-43) pathology. 4 key findings →
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. 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 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 →