Our study provides new insights into the brain distribution and cellular expression of an important risk factor associated with late-onset AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genome-wide association studies (GWAS) have provided insights into the genetic basis of complex diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the genome-wide association studies in Alzheimer's disease have highlighted inflammation as a driver of the disease rather than a consequence of the ongoing neurodegeneration, numerous studies have been performed to identify specific immune profiles associated with healthy, ageing, or diseased brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) is the second leading cause of dementia in individuals under age 65. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
To understand whether any human-specific new genes may be associated with human brain functions, we computationally screened the genetic vulnerable factors identified through Genome-Wide Association Studies and linkage analyses of nicotine addiction and found one human-specific de novo protein-coding gene, FLJ33706 (alternative gene symbol C20orf203). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies and functional genomics studies have linked specific cell types, genes, and pathways to Alzheimer's disease (AD) risk. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the current study, we used a novel single-cell whole genome sequencing (scWGS) approach to assess aneuploidy in isolated neurons from the frontal cortex of normal control individuals (n = 6) and patients with AD (n = 10). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Late onset Alzheimer's disease (LOAD) is a genetically complex and clinically heterogeneous disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive neurodegenerative disorder with high prevalence in old age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several proteins have been linked to neurodegenerative disorders (NDDs), but their molecular function is not completely understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathological studies have revealed the presence of a broad variety of inflammation-related proteins (complement factors, acute-phase proteins, pro-inflammatory cytokines) in Alzheimer's disease (AD) brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The power of fruit fly genetics is being deployed against some of the most intractable and economically significant problems in modern medicine, the neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder where the accumulation of amyloid plaques and the formation of tau tangles are the prominent pathological hallmarks. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For AD and PD, we found significant enrichment of heritability in annotations marking gene activity in immune cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Genome-wide association studies demonstrated that polymorphisms in the CD33/sialic acid-binding immunoglobulin-like lectin 3 gene are associated with late-onset Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Recent results from large-scale genomic projects suggest that allele frequencies, which are highly relevant for medical purposes, differ considerably across different populations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
With the assumption that common genetic signals obtained from different methodological platforms might serve as robust AD risk markers than candidates identified using single dimension approach, here we demonstrated an integrated genomic convergence approach for disease candidate gene prioritization from heterogeneous data sources linked to AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The successful discovery of genes that cause rare monogenic disorders has dominated our understanding of the genetic basis of neurodegenerative disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The small, calcium-sensor protein, calmodulin, is ubiquitously expressed and central to cell function in all cell types. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The findings from this study support an important role for SORL1 mutations in AD pathogenesis by way of altering Aβ levels and interfering with APP trafficking. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic or late-onset Alzheimer's disease (AD) is expected to affect 50% of individuals reaching 85 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the 1990s, the genetics of Alzheimer disease (AD) has been an active area of research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) primarily affect the motor and frontotemporal areas of the brain, respectively. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,980 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.
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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events