LP can be safely performed to study CSF biomarkers in DS. 1 key finding →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
LP can be safely performed to study CSF biomarkers in DS. 1 key finding →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with intellectual disabilities are at a higher risk for experiencing behavioral, emotional, and psychiatric problems in comparison with the general population. 2 key findings →
Participants: 255 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The brain metabolic decline in DS with age reflects Alzheimer's pathological processes and involves temporoparietal regions in a similar pattern to that found in other forms of AD. 4 key findings →
Participants: 71 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer's Disease Neuroimaging Initiative (ADNI) has fostered collaboration among researchers around the world, catalyzing innovation and accelerating progress in the field. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundMost adults with Down syndrome will develop Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein in the 21 st chromosome. 1 key finding →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Parkinson's disease (PD) is a neurodegenerative disorder that is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major components of which are filaments consisting of alpha-synuclein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The role of hypoperfusion in Alzheimer's disease (AD) is a vital component to understanding the pathogenesis of this disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI), the earliest clinically detectable phase of the trajectory toward dementia and Alzheimer's disease (AD), led to the need for even earlier detection and prevention of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI) is considered to be an early stage in the progression of Alzheimer's disease (AD) providing an opportunity to investigate brain pathogenesis prior to the onset of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Advances in AD biomarker research have demonstrated changes in amyloid-beta (Aβ), brain metabolism and other pathophysiologies prior to the onset of memory loss, with some markers possibly changing one or two decades earlier. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical hallmark of Alzheimer's disease (AD) is a gradual decline in cognitive function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synaptic integrity is now recognized as a central component of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia and mitigating amyloid-β (Aβ) levels may serve as a rational therapeutic avenue to slow AD progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Researchers have begun to characterize the subtle biological and cognitive processes that precede the clinical onset of Alzheimer disease (AD), and to set the stage for accelerated evaluation of experimental treatments to delay the onset, reduce the risk of, or completely prevent clinical decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The findings from this study add to the anatomical knowledge of hippocampal subregions in PD, allowing us to understand the unique functional contribution of each subfield. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite tremendous investments in understanding the complex molecular mechanisms underlying Alzheimer disease (AD), recent clinical trials have failed to show efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid precursor protein (APP) facilitates synapse formation in the developing brain, while beta-amyloid (Abeta) accumulation, which is associated with Alzheimer disease, results in synaptic loss and impaired neurotransmission. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Biochemical and genetic evidence establishes a central role of the amyloid precursor protein (APP) in Alzheimer disease (AD) pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Regional glucose hypometabolism is a defining feature of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The neural protein FE65 contains two types of protein-protein interaction modules: one WW binding domain and two phosphotyrosine binding domains. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in presenilins are responsible for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a genetic cause has been identified. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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.
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 27,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →