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
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
43/100
Expression of long-lasting synaptic plasticity and long-term memory requires protein synthesis, which can be repressed by phosphorylation of eukaryotic initiation factor 2 α-subunit (eIF2α). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is increasingly recognized as a condition shaped not only by central nervous system pathology but also by complex, bidirectional interactions between the gut, brain, and immune system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Optineurin (OPTN) is an autophagy adaptor protein involved in selective autophagy, including aggrephagy and mitophagy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks. 4 key findings →
Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is the most common form of dementia, characterized by two pathological hallmarks: amyloid-β plaques and neurofibrillary tangles. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Through the generation of humanized FUS mice expressing full-length human FUS, we identify that when expressed at near endogenous murine FUS levels, both wild-type and ALS-causing and frontotemporal dementia (FTD)-causing mutations complement the essential function(s) of murine FUS. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exonic and intronic mutations in Tau cause familial neurodegenerative syndromes characterized by frontotemporal dementia and dysfunction of multiple cortical and subcortical circuits. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Heterozygous, loss-of-function mutations in the granulin gene (GRN) encoding progranulin (PGRN) are a common cause of frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that microglial activation and the production of proinflammatory mediators by phospho-tau-positive neurons and glial cells may differentially contribute to neuronal death and disease progression in neurodegenerative tauopathies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of Alzheimer's disease (AD) and the commonest cause of dementia in the elderly remain incompletely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the microtubule-associated protein tau (MAPT) gene cause autosomal dominant frontotemporal lobar degeneration with tau inclusions (FTLD-tau). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E ( APOE ) genotype is the strongest prevalent genetic risk factor for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ageing of the human brain is a cause of cognitive decline in the elderly and the major risk factor for Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autophagy is a lysosomal degradative process used to recycle obsolete cellular constituents and eliminate damaged organelles and protein aggregates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An epidemic of age-associated cognitive decline, most commonly ascribed to neurodegenerative conditions such as Alzheimer's and Parkinson's disease, is causing healthcare costs to soar and devastating caregivers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the Presenilin genes (PSEN1 and PSEN2) are the major cause of familial Alzheimer's disease (AD), highlighting the importance of Presenilin (PS) in AD pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The synaptic regulator, kalirin, plays a key role in synaptic plasticity and formation of dendritic arbors and spines. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive deterioration of cognitive functions. 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
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →