28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Subjective cognitive decline (SCD) is increasingly recognised as a potential preclinical stage of Alzheimer's disease, yet the physiological mechanisms underlying its progression remain poorly understood. 4 key findings →
Design: longitudinal study Evidence: moderate
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Dementia syndromes involve cognitive but also early motor impairment. 3 key findings →
Design: longitudinal study Participants: 104 Evidence: moderate
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The relation between vitamin A (VA) level and cognitive function and the underlying mechanisms have not been thoroughly investigated. 2 key findings →
Design: cross-sectional Participants: 1,817 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As of a data cutoff of December 3, 2024, 243 participants were screened and 197 randomized in DIAN-TU-001 Tau NexGen trial (Cohort 1: 97; Cohort 2: 100). 5 key findings →
Participants: 243 Evidence: high
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There are many reports about the comorbidity of NPH and other neurodegenerative diseases1–3; the primary findings in neuropathological studies of patients with NPH include amyloid plaques and hyperphosphorylated tau protein inclusions.2,4 This suggests that proteinopathy may be one of the potential causes of NPH. 5 key findings →
Design: cohort study Participants: 50 Evidence: moderate
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GLP-1RA use was associated with lower risk of dementia (HR 0.80, 95% CI 0.71–0.91) and Alzheimer’s disease (HR 0.76, 95% CI 0.59–0.98) compared to DPP4is. 5 key findings →
Design: cohort study Participants: 12,351 Evidence: moderate
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Apathy was significantly more prevalent in dementia and MCI patients compared to HC. 5 key findings →
Design: cross-sectional Participants: 200 Evidence: moderate
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Epidemiological studies consistently indicate a two- to threefold increased risk of dementia among individuals with schizophrenia, although estimates vary due to diagnostic and ascertainment biases. 5 key findings →
Design: longitudinal study Evidence: moderate
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Our study reveals that PS in DLB is associated with specific deficits in attention and visuospatial/executive function, alongside more severe neuropsychiatric symptoms. 5 key findings →
Design: longitudinal study Participants: 35 Evidence: moderate
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Two clusters were identified in the microbiota at the phylum level that showed significant differences on a few microbiotas phylum. 4 key findings →
Participants: 292 Evidence: low
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Our study suggested that the long‐term exposure to air pollution was associated an increased risk of the transitions from health to incident cataract, dementia or the progression of both conditions. 2 key findings →
Participants: 409,608 Evidence: low
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Dementia risk is influenced by the social conditions in which people live. 5 key findings →
Evidence: low
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Our results elucidate the characteristics and genetic associations of p‐tau217 in a population‐based setting. 4 key findings →
Participants: 697 Evidence: low
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Emerging research found air pollution may be associated with incident Alzheimer’s disease (AD) and other dementias. 3 key findings →
Evidence: low
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The analysis tools and statistical methods used in large neuroimaging research studies differ from those applied in clinical contexts, making it unclear whether these techniques can be translated to a memory clinic setting. 5 key findings →
Participants: 213 Evidence: low
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Total serum TDP-43 levels increased by 16.5% (95% CI: 5.9%-27.9%, p = 0.0021) on postoperative day one compared to baseline levels. 5 key findings →
Participants: 25 Evidence: moderate
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Of the 500 eligible participants (71% female, 95% non-Latino White, mean [SD] age at cohort dementia onset = 88 [7] years, mean [SD] years from onset to death = 4 [3]), only 54% received a timely diagnosis. 5 key findings →
Evidence: moderate
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After adjusting for various factors, the incidence of Alzheimer dementia was significantly higher in the anosmia group compared to the control group (hazard ratio [HR], 1.15; 95% CI, 1.04-1.28). 4 key findings →
Design: cohort study Participants: 8,023 Evidence: moderate
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Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Lewy Body Disease (LBD), and related dementias, represent a global health challenge, particularly in aging populations. 5 key findings →
Evidence: low
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TANK-Binding Kinase 1 (TBK1) is involved in autophagy and immune signaling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) represents the most prevalent neurodegenerative disorder and leading cause of dementia worldwide, with its incidence rising dramatically in aging populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Menopause is a major biological transition that may influence women's late-life brain health. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, are characterized by the aggregation of α-synuclein. 1 key finding →
Evidence: low
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Among 90 participants included in the analyses, 34 had moderate to severe WMH. 5 key findings →
Participants: 154 Evidence: high
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These findings suggest that HB-CCT via Neurotablet can effectively enhance specific cognitive abilities in PD, supporting the role of digital, home-based interventions as feasible strategies to mitigate cognitive decline. 4 key findings →
Design: post-hoc analysis Evidence: high
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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 →