A strong genetic predisposition (60-80% of attributable risk) is present in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dysregulated proteostasis is a key feature of a variety of neurodegenerative disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As subjects with α-synuclein gene (SNCA) multiplication as well as point mutations develop familial Parkinson's disease and a genome-wide association study in Parkinson's disease has identified SNCA as a risk gene for Parkinson's disease, the increased expression of α-synuclein is closely associated with the aetiology of Parkinson's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies, including Alzheimer's disease (AD) and other neurodegenerative conditions, are defined by a pathological hallmark: neurofibrillary tangles (NFTs). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies identified the BIN1 locus as a leading modulator of genetic risk in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intervention in chronically activated microglia-mediated neuroinflammation is a novel approach to treat Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Alzheimer's disease (AD) is an age-related degenerative disease, which is characteristic by the deposition of senile plaques (SP) outside the cells, the neurofibrillary tangles (NFTs) inside the neurons, and the loss of synapse and neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Microglia play a crucial role in synaptic elimination by engulfing dystrophic neurons via triggering receptors expressed on myeloid cells 2 (TREM2). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a widespread neurodegenerative disorder and one of the major challenges for public health. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Alzheimer's disease (AD) is an age-related neurodegenerative disorder and the most common cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Cerebral atherosclerosis contributes to dementia via unclear processes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We performed proteomic analysis of neurofibrillary tangles (NFTs) obtained by laser capture microdissection from pyramidal neurons in hippocampal sector CA1 in patients with Alzheimer disease (AD) using liquid chromatography (LC)-mass spectrometry (MS)/MS. We discovered a total of 155 proteins in laser captured NFT's, 72 of which were identified by multiple unique peptides. 2 key findings →
Participants: 155 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) share key features, including accumulation of the RNA-binding protein TDP-43. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Preclinical changes that precede the onset of symptoms and eventual diagnosis of Alzheimer's disease (AD) are a target for potential preventive interventions. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
45/100
Microglial dysfunction is a key pathological feature of Alzheimer's disease (AD), but little is known about proteome-wide changes in microglia during the course of AD and their functional consequences. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
As more people live longer, age-related neurodegenerative diseases are an increasingly important societal health issue. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Quantitative proteomics analysis of cortical samples of 10 Alzheimer's disease (AD) brains versus 10 normally aged brains was performed by following the accurate mass and time tag (AMT) approach with the high resolution LTQ Orbitrap mass spectrometer. 4 key findings →
Participants: 197 Evidence: low
Full summary, score breakdown and related studies → Original source
The central nervous system has a pattern of gene expression that is closely regulated with respect to functional and anatomical regions. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) maintains brain homeostasis by controlling traffic of molecules from the circulation into the brain. 1 key finding →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
There is a fundamental gap in understanding the consequences of tau-ribosome interactions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
GABA B receptors (GBRs) are key regulators of synaptic release but little is known about trafficking mechanisms that control their presynaptic abundance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Transcription factor EB (TFEB) mediates gene expression through binding to the coordinated lysosome expression and regulation (CLEAR) sequence. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study represents the first epigenome-wide association study of both DNA methylation and hydroxymethylation in Alzheimer's disease entorhinal cortex. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The single nucleotide polymorphism (SNP) rs744373 in the bridging integrator-1 gene (BIN1) is a risk factor for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The abnormal accumulation of amyloid-β and tau targets specific spatial networks in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,313 studies in this tag that have a study page, 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.
- Melanopsin retinal ganglion cell loss in Alzheimer disease
- Early astrocytic atrophy in the entorhinal cortex of a triple transgenic animal model of Alzheimer's disease
- Autonomous AI-Driven Nanoscale Spatial Mapping Reveals Novel Targets and Ternary Architectures in 5xFAD Alzheimer's Disease Model
- APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies
- sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's disease
- High-Dimensional Single-Cell Mapping of Central Nervous System Immune Cells Reveals Distinct Myeloid Subsets in Health, Aging, and Disease
- Tau reduction prevents Abeta-induced defects in axonal transport
- Inflammatory processes induce beta-amyloid precursor protein changes in mouse brain
- Conscientiousness and the incidence of Alzheimer disease and mild cognitive impairment
- [18F]-AV-1451 binding profile in chronic traumatic encephalopathy: a postmortem case series
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →