27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are neurodegenerative diseases with clinical and pathological overlap. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies of post-mortem tissue have shown that the location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regions of massive neuronal death, severe cytological abnormalities, and markers of caspase activation and apoptosis, leading to the idea that tangles cause neurodegeneration in Alzheimer's disease and tau-related frontotemporal dementia. 2 key findings →
Evidence: low
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Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. 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
Full summary, score breakdown and related studies → Original source Free full text
Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Australian Imaging, Biomarkers and Lifestyle (AIBL) study performed (11)C-Pittsburgh Compound B (PiB) scans in 177 healthy controls (HC), 57 mild cognitive impairment (MCI) subjects, and 53 mild Alzheimer's disease (AD) patients. 5 key findings →
Evidence: low
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White matter hyperintensities predict an increased risk of stroke, dementia, and death.
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This prognostic index provides an accurate and transportable method of stratifying 1-year death risk in PP. 3 key findings →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source
The ADRQL is a valid indicator of QOL in NH residents with advanced dementia. 2 key findings →
Design: cross-sectional Participants: 119 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this analysis, two single nucleotide polymorphisms in a locus on chromosome 9p21.2 were associated with ALS: rs3849942 (p=2·22×10(-6); odds ratio [OR] 1·39, 95% CI 1·21-1·59) and rs2814707 (p=3·32×10(-6); 1·38, 1·20-1·58). 5 key findings →
Participants: 599 Evidence: moderate
Full summary, score breakdown and related studies → Original source
High HDL-C levels in elderly individuals may be associated with a decreased risk of AD. 3 key findings →
Design: cohort study Evidence: moderate
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Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →
Participants: 399 Evidence: low
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A subgroup of patients with Alzheimer disease with extreme levels of CSF biomarkers exhibits worse clinical outcomes over time, including faster progression of cognitive deficits, no response to ChEI treatment, and a higher mortality. 1 key finding →
Participants: 151 Evidence: low
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Unlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype. 3 key findings →
Participants: 312 Evidence: low
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This enlarged study confirms earlier findings that statin therapy in early old age, but not in late age, may be associated with a lower risk of AD. 4 key findings →
Participants: 3,099 Evidence: moderate
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MCI diagnosis frequencies are substantively affected by the stringency of the criteria, but the relative rankings of MCI subtype diagnoses are fairly consistent regardless of the stringency of the criteria. 5 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
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The strong correlation between hippocampal atrophy and beta-amyloid (Abeta) burden in the Pittsburgh compound B-positive healthy control group suggests that Abeta deposition in the inferior temporal neocortex is related to hippocampal synaptic and neuronal degeneration. 3 key findings →
Participants: 32 Evidence: low
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The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion. 2 key findings →
Design: cross-sectional Participants: 397 Evidence: moderate
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We examined the association of type 2 diabetes mellitus to function in different cognitive systems in older black and white persons. 2 key findings →
Design: cohort study Participants: 1,437 Evidence: moderate
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The ongoing development of robotics on the one hand and, on the other hand, the foreseen relative growth in number of elderly individuals suffering from dementia, raises the question of which contribution robotics could have to rationalize and maintain, or even improve the quality of care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found reduced ¹²³I-FP-CIT binding in the striatum (p=0·045) in 17 (40%) of 43 participants compared with 18 controls, and substantia nigra hyperechogenicity in 14 (36%) of 39 participants with IRBD, compared with 16 (11%) of 149 controls (p=0·0002). 5 key findings →
Participants: 43 Evidence: low
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Tar DNA Binding Protein-43 (TDP-43) is a principle component of inclusions in many cases of frontotemporal lobar degeneration (FTLD-U) and amyotrophic lateral sclerosis (ALS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A CDR rating of 0.5 (uncertain/very mild dementia) was obtained by 27.6% of participants, whereas 1.2% had CDR ≥ 1 (mild or moderate dementia). 1 key finding →
Design: cross-sectional Participants: 2,036 Evidence: moderate
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Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal β-amyloid deposition in addition to diffuse Lewy bodies (α-synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Brain atrophy and altered CSF levels of amyloid beta (Abeta(42)) and the microtubule-associated protein tau are potent biomarkers of Alzheimer's disease (AD)-related pathology. 4 key findings →
Design: longitudinal study Evidence: moderate
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 →