TREM2 is a receptor for lipids expressed in microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
TREM2 is a receptor for lipids expressed in microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synaptic loss is an early pathologic substrate of Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 38 Evidence: moderate
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Delirium is a profound neuropsychiatric disturbance precipitated by acute illness. 4 key findings →
Design: longitudinal study Participants: 465 Evidence: moderate
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Cerebral amyloid angiopathy (CAA), limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC) and Lewy bodies occur in the absence of clinical and neuropathological Alzheimer's disease, but their prevalence and severity dramatically increase in Alzheimer's disease. 4 key findings →
Participants: 522 Evidence: moderate
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Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments. 4 key findings →
Design: longitudinal study Participants: 389 Evidence: moderate
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Amyloid-beta peptide (Abeta) has a key role in the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Alzheimer's disease is characterized by β-amyloid plaques and tau tangles. 4 key findings →
Participants: 88 Evidence: moderate
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Alzheimer's disease (AD) is the most prevalent cause of dementia 1 . 4 key findings →
Evidence: low
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Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD. 4 key findings →
Evidence: low
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Recent studies suggest the existence of brain-first and body-first subtypes within the Lewy body disorder (LBD) spectrum, including Parkinson's disease. 1 key finding →
Participants: 173 Evidence: low
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The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr. 5 key findings →
Design: cohort study Participants: 13 Evidence: moderate
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Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion. 5 key findings →
Design: cross-sectional Participants: 1,393 Evidence: moderate
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
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Alzheimer's disease (AD) has a strong genetic component, with APOE ε4 being the most established risk factor through its effects on beta-amyloid (Aβ) metabolism and microglial function. 5 key findings →
Participants: 500,000 Evidence: moderate
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The Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed a practical and standardized neuropathology protocol for the postmortem assessment of dementia and control subjects. 5 key findings →
Evidence: low
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Despite continuing debate about the amyloid β-protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early, often initiating factor in Alzheimer's disease (AD). 5 key findings →
Evidence: low
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We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life. 2 key findings →
Evidence: low
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People with type 2 diabetes mellitus (T2DM) are at increased risk of mild cognitive impairment and dementia. 5 key findings →
Design: meta-analysis Evidence: high
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Brain regions with higher synaptic density are associated with a higher 18F-AV-1451 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminishes with disease severity. 1 key finding →
Design: cross-sectional Participants: 12 Evidence: moderate
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The loss of occlusal support may lead to cognitive dysfunction through the reduction of chewing-related stimuli, aggravation of nerve damage, and long-term inflammatory stress. 1 key finding →
Design: systematic review Participants: 1,317 Evidence: high
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The analysis included 26 original articles describing (1050 rodents) with AD-like symptoms. 5 key findings →
Design: systematic review Participants: 26 Evidence: high
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Baseline plasma MCP-1 levels were associated with longitudinal declines in overall cognitive and episodic memory performance in older adults over a 4-year follow-up. 5 key findings →
Design: longitudinal study Participants: 1,097 Evidence: moderate
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Researchers developed an adeno-associated virus-based model to study tau propagation from the entorhinal cortex to the dentate gyrus. 2 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Free full text
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →