27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The extent and location of neuronal losses necessary or sufficient to produce dementia in patients with Alzheimer's Disease (AD) is unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Breakthroughs in the development of highly accurate fluid and neuroimaging biomarkers have catalysed the conceptual transformation of Alzheimer disease (AD) from the traditional clinical symptom-based definition to a clinical-biological construct along a temporal continuum. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer's disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). 1 key finding →
Evidence: low
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
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative disorders characterized by the accumulation of abnormal tau protein leading to cognitive and/or motor dysfunction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule-associated protein tau oligomerizes, but the actions of oligomeric tau (oTau) are unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly in attention, learning and memory, and higher-order executive functions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are often classified based on the abnormal accumulation of synuclein or tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the foremost type of dementia that afflicts considerable morbidity and mortality in aged population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The incidence of dementia is higher in diabetic patients, but no effective treatment has been developed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium is an acute, severe neuropsychiatric syndrome, characterized by cognitive deficits, that is highly prevalent in aging and dementia and is frequently precipitated by peripheral infections. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the commonest cause of dementia in the elderly, but its pathological determinants are still debated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed the prevalence of common altered brain proteins in 296 cognitively unimpaired subjects ranging from age 50 to 102 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study supports previous findings of heterogenous pathology in essential tremor (ET). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and frontotemporal dementias (FTD), are considered distinct entities, however, there is increasing evidence of an overlap from the clinical, pathological and genetic points of view. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review highlights the progression of biological changes underlying AD and their association with the clinical syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
C9orf72 repeat expansions cause inherited amyotrophic lateral sclerosis (ALS)/frontotemporal dementia (FTD) and result in both loss of C9orf72 protein expression and production of potentially toxic RNA and dipeptide repeat proteins. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta (Aβ) is a peptide of 39-43 amino acids found in large amounts and forming deposits in the brain tissue of patients with Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most prevalent tauopathy and cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A small, orally available natural product penetrates into the brain in vivo to rescue the memory impairment produced by soluble Abeta oligomers through a mechanism that restores hippocampal synaptic plasticity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Each of these subtypes is associated with differential 18 F-FDG PET findings. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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 →