Activation of glial cells and neuroinflammation play an important role in the onset and development of Alzheimer's disease (AD). 4 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.
Nasu-Hakola disease (NHD) was first reported separately by Nasu and Hakola around the same time in the 1970s. It is an autosomal recessive inherited disorder characterized by progressive dementia and repeated pathological fractures during adolescence. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Microglia play major roles in initiation, coordination and execution of innate immunity in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
40/100
Falls before dementia were linked to a higher risk of dementia. 3 key findings →
Participants: 403,502 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
> 0.95) and is present in all African ancestry tested. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overall SNP‐based heritability estimates using this restricted set of variants varied: AA ( h 2 = 0.13, SE=0.05), NHW ( h 2 = 0.14, SE=0.01), AsA ( h 2 = 0.29, SE=0.09) and HL ( h 2 = 0.48, SE=0.17). 2 key findings →
Participants: 6,343 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Finally, at the RHOJ locus, the rare allele was associated with increased tTau ( p ‐value=4.74×10 ‐05 ) and pTau181 ( p ‐value=4.07×10 ‐07 ), and decreased Aβ42/40 ratio ( p ‐value=4.32×10 ‐05 ). 2 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Identity-by-descent (IBD) mapping provides complementary signals to genome-wide association studies (GWASs) when multiple causal haplotypes or variants are present but not directly tested. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One hundred and eighteen years have passed since Alzheimer's disease (AD) was first diagnosed by Alois Alzheimer as a multifactorial and complex neurodegenerative disorder with psychiatric components. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The growing prevalence of dementia emphasizes the need for effective prevention strategies. 4 key findings →
Participants: 289 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overexpression of apoE isoforms induces differential effects in the apoE4-TR background: apoE4 decreases apoE lipidation and enhances Aβ accumulation, whereas apoE2 has the opposite effects. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases, sporadic or familial, mainly characterized by dementia and parkinsonism associated to atrophy of the frontotemporal cortex and the basal ganglia, with deposition of abnormal tau in brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Changes of the microtubule-associated protein tau are central in Alzheimer's disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) has been associated with toxic intracellular aggregates of hyperphosphorylated tau (FTLD-tau). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the gene MAPT encoding tau, a microtubules-associated protein, cause a subtype of familial neurodegenerative disorder, known as frontotemporal lobar degeneration tauopathy (FTLD-Tau), which presents with dementia and is characterized by atrophy in the frontal and temporal lobes of the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
We report a case of rapidly progressive frontotemporal dementia presenting at age 33 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report the first case of neuropathologically verified parkinsonism-dementia complex of the Kii peninsula, together with the patient's brother, who had amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Little is known about how changes in DNA methylation mediate risk for human diseases including dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Methylation is a post-translational modification that can affect numerous features of proteins, notably cellular localization, turnover, activity, and molecular interactions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A family is described with familial myoclonic epilepsy associated with mitochondrial myopathy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is the first study to show aberrant regulation of the protein synthesis machinery in the suicide brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that in patients with schizophrenia spectrum disorders, hippocampal volume is influenced in part by schizophrenia susceptibility genes and an interaction of these genes with fetal hypoxia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,549 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.
- Complete genomic screen in late-onset familial Alzheimer disease. Evidence for a new locus on chromosome 12
- VCP disease associated with myopathy, Paget disease of bone and frontotemporal dementia: review of a unique disorder
- Sex differences in the clinical manifestation of autosomal dominant frontotemporal dementia
- Disease-modifying effects of TMEM106B in genetic frontotemporal dementia: a longitudinal GENFI study
- Tau proteins with FTDP-17 mutations have a reduced ability to promote microtubule assembly
- Clinical and attitudinal outcomes of a personalized, multimodal lifestyle intervention for Alzheimer's disease prevention in high-risk, cognitively normal older adults in north Alabama: A pilot study
- The Caenorhabditis elegans IMPAS gene, imp-2, is essential for development and is functionally distinct from related presenilins
- Meat consumption and risk of incident dementia: cohort study of 493,888 UK Biobank participants
- RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia
- Genome-wide prediction of imprinted murine genes
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 →