APP processing and amyloid-β production play a central role in Alzheimer disease pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
APP processing and amyloid-β production play a central role in Alzheimer disease pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
According to the ' amyloid cascade hypothesis of Alzheimer's disease ' first proposed about 16 years ago, the accumulation of Aβ peptides in the human central nervous system (CNS) is the primary influence driving Alzheimer's disease (AD) pathogenesis, and Aβ peptide accretion is the result of an imbalance between Aβ peptide production and clearance. 2 key findings →
Evidence: low
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The triggering receptor expressed on myeloid cells (TREM) 2 is a member of the immunoglobulin superfamily of receptors and mediates signaling in immune cells via engagement of its co-receptor DNAX-activating protein of 12 kDa (DAP12). 3 key findings →
Evidence: low
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Preeclampsia is a multisystemic, pregnancy-specific disorder united by new-onset hypertension but with considerable variation in clinical manifestation, onset, and severity. 4 key findings →
Evidence: low
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Aging is regarded as a major risk factor for neurodegenerative diseases. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. 4 key findings →
Evidence: low
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Triggering receptor expressed on myeloid cells 2 (TREM2) is involved in nonmalignant pathological processes. 4 key findings →
Evidence: low
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Aging is associated with an exaggerated response to peripheral inflammatory challenges together with behavioral and cognitive deficits. 4 key findings →
Evidence: low
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The expression of the triggering receptor on myeloid cell-2 (TREM2) knockdown in microglia from the lateral habenula (LHb) reportedly induces depression-like behaviors in mice. 4 key findings →
Evidence: low
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Neuroinflammation plays a role in the aetiopathogenesis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Traumatic brain injury (TBI) is an unfortunately common event in military life. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau. 4 key findings →
Evidence: low
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Stroke is the second most common cause of death and permanent disability. 4 key findings →
Evidence: low
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Alcohol use disorder (AUD) pathology features pro-inflammatory gene induction and microglial activation. 4 key findings →
Evidence: low
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In CN subjects, study-wide significant (P -9 ) loci were identified for total tau near SRRM4 and C14orf79 and for hippocampal volume near MTUS1. 4 key findings →
Evidence: low
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Crocus sativus L. natural compounds have been extensively used in traditional medicine for thousands of years. 4 key findings →
Evidence: low
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We retrospectively assessed participants with atypical and/or early-onset dementia evaluated at a tertiary care memory clinic. 4 key findings →
Evidence: low
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This observational study included 290 cognitively unimpaired (CU) participants with a family history (FH) of clinically diagnosed sporadic AD (age 49-73 years) from the Alzheimer's and Families (ALFA) study. [ 18 F]flutemetamol-PET standardized uptake value ratios, CSF β-amyloid 42/40 ratio, and phosphorylated tau were used as AD biomarkers. 4 key findings →
Participants: 290 Evidence: low
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The authors sought to examine the impact of the K-variant of butyrylcholinesterase (BCHE-K) carrier status on age-at-diagnosis of Alzheimer disease (AD) in APOE4 carriers. 4 key findings →
Design: post-hoc analysis Participants: 33 Evidence: low
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Creatine transporter deficiency (CTD) is a rare X-linked disorder of creatine transport caused by pathogenic variants in SLC6A8 (Xq28). 4 key findings →
Participants: 12 Evidence: moderate
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Alzheimer's disease (AD) is the most common neurodegenerative disease. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is the most common neurodegenerative disease and typically affects patients older than age 65. 4 key findings →
Evidence: low
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The clinical impact of Alzheimer's disease pathology at biopsy was investigated in 56 cognitively impaired patients undergoing shunt surgery for idiopathic normal pressure hydrocephalus (NPH). 4 key findings →
Evidence: low
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In the study by Derogatis et al., which included patients with all stages of cancer, 47% of the patients met the DSM-III criteria for a psychiatric disorder, with adjustment disorders being the most common. 4 key findings →
Participants: 26 Evidence: low
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Performance on cognitive tests can be affected by age, education, and also selection bias. 4 key findings →
Evidence: moderate
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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.
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 →