27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Caregivers in the control conditions reported significantly worsening sleep efficiency whereas in comparison, those in the active conditions reported improving sleep efficiency. 4 key findings →
Evidence: low
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The development of cerebrospinal fluid and blood-based biomarkers for Alzheimer disease (AD) and related disorders is rapidly progressing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The associations of lower foveal capillary density with cerebral WMH and amyloid positivity suggest that further research is warranted to evaluate for shared mechanisms of disease between small vessel disease and AD pathologies. 5 key findings →
Participants: 41 Evidence: low
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We tested association of nine late-onset Alzheimer's disease (LOAD) risk variants from genome-wide association studies (GWAS) with memory and progression to mild cognitive impairment (MCI) or LOAD (MCI/LOAD) in older Caucasians, cognitively normal at baseline and longitudinally evaluated at Mayo Clinic Rochester and Jacksonville (n>2000). 5 key findings →
Evidence: low
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Many insults, including trauma, ischemia, infection, inflammation, and neurodegeneration, result in irreversible damage to the central nervous system. 3 key findings →
Design: clinical trial Evidence: high
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In 1994-1995, a screening and examination survey was conducted to ascertain the prevalence of dementia, Parkinson's disease and stroke in two urban communities and one rural community of central Spain. 3 key findings →
Evidence: low
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Among people with multiple sclerosis, cognitive impairment occurs commonly and is a potent predictor of disability. 4 key findings →
Evidence: moderate
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Higher serum GFAP, YKL-40, sCD14, and NfL were associat 4 key findings →
Participants: 3,082 Evidence: low
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Blood-based biomarkers are increasingly used to characterize Alzheimer's disease (AD)-related pathology, yet substantial heterogeneity exists in how biomarker burden relates to cognitive performance. 4 key findings →
Design: cross-sectional Participants: 348 Evidence: low
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Amyloid-targeted monoclonal antibody therapies have introduced a new era in the treatment of early Alzheimer disease. 2 key findings →
Evidence: low
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Aggregation of the microtubule-binding protein tau is the histopathological hallmark of Alzheimer's disease (AD) and other neurodegenerative diseases, which are collectively known as tauopathies. 5 key findings →
Evidence: low
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Neighborhood deprivation was associated with poorer cognition (r = 0.36, p < 0.001), greater prevalence of modifiable risk factors (r = 0.36, p < 0.001), and greater SVD burden (β = 0.18, p = 0.008). 4 key findings →
Evidence: low
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In these, at least one cardinal symptom or sign of PSP later emerges, associated with smaller midbrain volume and increased pons/midbrain ratio. 4 key findings →
Evidence: low
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We describe a right-handed man who developed progressive nonfluent aphasia and apraxia of speech beginning at age 71. 2 key findings →
Evidence: low
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Accurate diagnosis of frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance remains challenging due to lack of clinical characterization, and standardized terminology. 4 key findings →
Evidence: low
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Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Using a unique dataset of the same participants scanned close in time on different scanner and protocols, we found that (1) MMD measurements were useful to test the need/improvement due to harmonization; (2) ComBat was not substantially better at creating compatible distributions between scanner vendors than Deming regression, and both were sometimes inadequate. 4 key findings →
Participants: 53 Evidence: low
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Cotton wool plaques (CWP) are large, ball-like plaques lacking dense amyloid cores that displace adjacent structures. 3 key findings →
Evidence: low
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We aim to compare the biological staging of Alzheimer Disease using two different tau PET tracers. 1 key finding →
Evidence: low
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These findings suggest probable amyloid association with early microglial activation, while tau pathology is closely tied to wider distribution of neuroinflammation. 3 key findings →
Evidence: low
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The C9orf72 hexanucleotide repeat expansion mutation is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, but its cell type-specific effects on energy metabolism and immune pathways remain poorly understood. 3 key findings →
Evidence: low
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Several concepts, which in the aggregate get might be used to account for "resilience" against age- and disease-related changes, have been the subject of much research.
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Inexpensive, non-invasive tools for assessing Alzheimer-type pathophysiologies are needed. 1 key finding →
Evidence: low
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There are many who feel that the achievement of a disease-modifying (DM) designation for a drug is an important goal in Alzheimer disease (AD) therapeutics. 5 key findings →
Evidence: high
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The analyses of the community‐based U.S. POINTER indicate that AA/B individuals present differences in AD and related dementia biomarker values. nHW had higher fully adjusted cognitive scores. 5 key findings →
Participants: 644 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 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 →