Our results show that genotype, AOF, and sex contributed to AD-like pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
35/100
Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence highlights the central role of peripheral immune-metabolic regulation in the pathogenesis of Alzheimer's disease and related dementias (ADRD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
35/100
Emerging evidence transcends the traditional central nervous system (CNS)-centric perspective, revealing that neutrophils, red blood cells (RBCs), and platelets may play critical roles in AD pathogenesis by modulating systemic inflammatory responses, disrupting blood-brain barrier integrity, and participating in the CNS-peripheral interactions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is neuropathologically characterized by neuritic plaques and neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The accuracy of α-synuclein-SAA for DLB was 87% (95% confidence interval [CI]: 77% to 98%) in CSF, 85% (95% CI: 75% to 98%) in skin, 58% (95% CI: 47% to 69%) in olfactory mucosa, and 59% (95% CI: 51% to 66%) in urine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found a moderate yet significant reduction in Aβ plaque size in male 5×FAD × mAPPA673T compared with 5×FAD mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Most Alzheimer disease (AD) susceptibility genes have poorly understood roles in the central nervous system (CNS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies were undertaken to assess the extent to which messenger RNA prepared from the postmortem Alzheimer's disease (AD) brain can be used for the successful preparation of a recombinant cDNA library. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mutations in the presenilin 1 (PS1) gene (PSEN1) are associated with familial Alzheimer disease (FAD). 4 key findings →
Evidence: low
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Among 15,346 White, 829 Latino, 637 Black/African American, and 321 Asian individuals, 51% were female, mean age was 75.7 years, 535 (3.8%) resided in ADI 91 to 100 decile, and 61.6% were amyloid PET positive. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The APOE (apolipoprotein E) ε4 allele is the strongest known genetic risk factor for sporadic Alzheimer disease (AD) and for brain amyloidosis, an early marker of disease pathophysiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that sexual differentiation in early life has modest effects on adult development of AD in females, a relationship that appeared stronger in the context of APOE4 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the colocalization of cis-eQTL and GWAS signals for Hispanics, we observed a high posterior probability (posterior prob = 0.9947) for the upstream gene variant rs755980338 on chromosome 11, which locally regulates EHD1 gene (GWAS p-value = 0.009, cis-eQTL p-value = 0.0041). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundEpigenetic mechanisms, particularly histone modifications at gene promoters, are crucial for controlling gene transcription. 4 key findings →
Evidence: low
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This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment. 1 key finding →
Evidence: low
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Cerebral amyloid angiopathy (CAA), which is prevalent among older adults, constitutes a major cause of brain hemorrhage, dementia, and cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by synaptic dysfunction, neuroinflammation, and cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive memory loss and cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous studies have shown a marked decline in neuronal and an increase in glial gene expression in Alzheimer's disease (AD) neocortex. 2 key findings →
Evidence: low
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To determine the relationship between regional brain edema caused by anti-amyloid monoclonal antibody therapy (ARIA-E) and the degree of regional β-amyloid (Aβ) positron emission tomography (PET) signal reduction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
From across this tag
9 of the 1,348 studies in this tag, 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 9. The same 9 appear here every time.
- The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy of Alzheimer's Disease and Other Neurodegenerative Disorders
- ApoE4 Upregulates GSK ‐3β to Aggravate Alzheimer‐Like Pathologies and Cognitive Impairment in Type 2 Diabetic Mice
- Astrocytes: implications for neuroinflammatory pathogenesis of Alzheimer's disease
- Integrative brain transcriptome analysis links complement component 4 and HSPA2 to the APOE ε2 protective effect in Alzheimer disease
- Lack of ABCA1 considerably decreases brain ApoE level and increases amyloid deposition in APP23 mice
- Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein
- Novel sex‐specific candidate loci associated with Alzheimer disease identified through sex‐aware multi‐ancestry genome‐wide meta‐analysis
- Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: insights into the development of Alzheimer's disease
- Platelet coagulation factor XIa-inhibitor, a form of Alzheimer amyloid precursor protein
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 27,780 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →