Apolipoprotein E ε4 (APOE ε4) bring the higher risk of Alzheimer' Disease (AD). 4 key findings →
Participants: 1,610 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Inclusion body myopathy (IBM) associated with Paget disease of the bone (PDB) and frontotemporal dementia (FTD) (now called IBMPFD), is a progressive autosomal dominant disorder that was recently identified as being caused by mutations in the VCP (p97 or CDC48) gene which plays a key role in the ubiquitin-proteasome dependent degradation of cytosolic proteins and in the retro translocation of misfolded proteins from the endoplasmic reticulum into the cytoplasm. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nowadays, there is an unmet need for reliable and minimally-invasive diagnosis tools capable of detecting Alzheimer's disease at early stages. 3 key findings →
Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD), the most common dementing syndrome in the United States, is currently established by the presence of amyloid-β and tau protein biomarkers in the setting of clinical cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Machine learning enables scalable quantification of neuropathology, offering deeper phenotyping of Alzheimer's disease (AD). 4 key findings →
Participants: 273 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight normative modelling's utility in revealing the complex interplay among sex, age, and AD risk in shaping brain structure and cognition in later life. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A positive family history was reported in 42% of patients in the Alzheimer disease cohort, 48% of patients in the frontotemporal dementia cohort, and 34% in those with other dementia types. 5 key findings →
Participants: 701 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Environmental and lifestyle factors significantly contribute to gynecological cancers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundPopulation ageing in Africa will increase the burden of Alzheimer's disease and related dementias within the next few decades. 1 key finding →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
43/100
We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
FTD subjects exhibited increased plasma levels of gangliosides (GM3(d18:1_16:0), GM3(d18:1_24:1)), ceramide Cer(d18:1_23:0), and select polyunsaturated triacylglycerols. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accurate dementia risk prediction is challenging, and may be facilitated by better use of imaging and genetic data, including their complex interactions. 1 key finding →
Design: post-hoc analysis Participants: 3,521 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variants increase the risk of neurocognitive disorders in later life, including vascular dementia (VaD) and Alzheimer’s disease (AD), but the precise relationships between genetic risk factors and underlying disease etiologies are not well understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular contributions to cognitive impairment and dementia (VCID) represent a major public health challenge in the aging population, with age-related cerebromicrovascular dysfunction playing a critical role in its development. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous data from familial AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein suggest that the long form of Abeta peptide, Abeta42, is selectively increased in these circumstances. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Our results suggest significant mechanistic overlap between AD and COVID-19, centered on neuroinflammation and microvascular injury. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) constitutes the most prominent form of dementia among elderly individuals worldwide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Splice-site and missense mutations have been identified in tau associated with frontotemporal dementia with parkinsonism linked to chromosome 17. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial frontotemporal dementia (FTD), characterized by tau-negative, ubiquitin-positive inclusions at autopsy, is linked to a chromosomal region at 17q21 (FTDU-17), encompassing the gene encoding the microtubule associated protein tau, MAPT. 2 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this paper was to investigate the association of three well-recognised dietary patterns with cognitive change over a 3-year period. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive impairment is a common non-motor symptom in Parkinson's Disease (PD) and an important source of patient disability and caregiver burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,521 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 10. The same 10 appear here every time.
- The two faces of protein misfolding: gain- and loss-of-function in neurodegenerative diseases
- Metabolic syndrome and risk for incident Alzheimer's disease or vascular dementia: the Three-City Study
- MAPT mutations, tauopathy, and mechanisms of neurodegeneration
- Local genetic covariance analysis with lipid traits identifies novel loci for early-onset Alzheimer’s Disease
- Apolipoprotein E Induces Lipid Accumulation Through Dgat2 That Is Prevented with Time-Restricted Feeding in Drosophila
- Primary Tau Pathology, Not Copathology, Correlates With Clinical Symptoms in PSP and CBD
- Improved discrimination of AD patients using beta-amyloid(1-42) and tau levels in CSF
- Discovery of sexual dimorphisms in metabolic and genetic biomarkers
- Clinical and demographic factors modify the association between plasma phosphorylated tau-181 and cognition
- The BDNF Val66Met polymorphism impacts parahippocampal and amygdala volume in healthy humans: incremental support for a genetic risk factor for depression
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 27,380 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.
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 27,380 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 →