Alzheimer disease (AD) is the most common type of dementia and is currently estimated to affect 6.2 million Americans. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is characterized by the presence of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs), neuronal and synaptic loss and inflammation of the central nervous system (CNS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CD33/Siglec 3 is a myeloid lineage cell surface receptor that is known to regulate microglia activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
No significant causal association was found between SLE and any type of dementia, including Alzheimer's disease, vascular dementia, frontotemporal dementia, and dementia with Lewy bodies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anorexia nervosa (AN) is a devastating disorder with evidence of underexplored heritability. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies proposed the Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a receptor expressed in myeloid cells including microglia in brain and osteoclasts in bone, as a link between brain and bone disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TREM2 (Triggering receptor expressed on myeloid cells 2) is the causative gene for Nasu-Hakola disease, which is characterized by multiple bone cysts and leukoencephalopathy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) promotes several Alzheimer's disease-like pathological features, including microtubule-associated protein tau (MAPT) accumulation within neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is a progressive neurological disorder marked by cardinal clinical symptoms such as rigor, tremor, and akinesia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common form of dementia, accounting for as much as three-quarters of cases globally with individuals in low- and middle-income countries being worst affected. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Four out of 10 TREM2 mutant variants have been identified in the analyzed groups, namely rs75932628 C > T (R47H), rs142232675 C > T (D87N), rs143332484 C > T (R62H), and rs2234253 G > T (T96K). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapses are bridges for information transmission in the central nervous system (CNS), and synaptic plasticity is fundamental for the normal function of synapses, contributing substantially to learning and memory. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cancer continues to be a substantial health concern and a leading cause of death in the United States and around the world. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The receptor Triggering Receptor Expressed on Myeloid cells 2 (TREM2) is associated with several neurodegenerative diseases including Alzheimer's Disease and TREM2 stimulation represents a novel therapeutic opportunity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The presenilin genes (PSEN1 and PSEN2) are mainly responsible for causing early-onset familial Alzheimer's disease, harboring ~300 causative mutations, and representing ~90% of all mutations associated with a very aggressive disease form. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We studied small vessel disease (SVD) pathology in Familial Alzheimer's disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer's disease (SAD) as a positive control for Alzheimer's pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The established causal genes in Alzheimer's disease (AD), APP, PSEN1, and PSEN2, are functionally characterized using biomarkers, capturing an in vivo profile reflecting the disease's initial preclinical phase. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified five novel variants in the presenilin1 (PSEN1) gene from Brazilian and Mexican families. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The three female patients had an age of onset of symptoms of 38-51 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilin 1 (PSEN1) mutations are a major cause of familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau aggregation in neurofibrillary tangles (NFTs) is closely associated with neurodegeneration and cognitive decline in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The molecular diversity of glia in the human hippocampus and their temporal dynamics over the lifespan remain largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified several DEGs in both neuronal and glial cell subtypes in comparisons of wild type (WT) versus 5XFAD and WT versus T2KO mice, including Ttr, Fth1, Pcsk1n, Malat1, Rpl37, Rtn1, Sepw1, Uba52, Mbp, Arl6ip5, Gm26917, Vwa1, and Pgrmc1. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epigenetic age has emerged as an important biomarker of biological ageing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accelerated aging is a hallmark of Down syndrome (DS), with adults experiencing early-onset Alzheimer's disease and premature aging of the skin, hair, and immune and endocrine systems. 4 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 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 →