30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although multiple CHCHD10 mutations are associated with the spectrum of familial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neither the normal function of endogenous CHCHD10 nor its role in the pathological milieu (that is, TDP-43 pathology) of FTD/ALS have been investigated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An unusually high frequency of atypical Parkinson syndrome has been delineated over the last 5 years in the French West Indies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Systemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) are clinically and neuropathologically highly related α-synucleinopathies that collectively constitute the second leading cause of neurodegenerative dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A 59-year-old man developed problems with reading and driving. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detailed molecular pathology studies and clinicopathological phenotyping of familial amyotrophic lateral sclerosis (FALS) with characterised mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1) will yield important insights into the pathogenesis of motor neuron degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prostate cancer (PCa) is one of the most prevalent malignancies affecting males worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Memory loss in Alzheimer's disease (AD) is attributed to pervasive weakening and loss of synapses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early life experience influences stress reactivity and mental health through effects on cognitive-emotional functions that are, in part, linked to gene expression in the dorsal and ventral hippocampus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Major Depressive Disorder (MDD) is a common psychiatric disorder for which available medications are often not effective. 4 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) comprises pathological processes of the small vessels in the brain that may manifest clinically as stroke, cognitive impairment, dementia, or gait disturbance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
IR among asymptomatic APOEɛ4 carriers was associated with higher P-Tau181 and T-Tau in late-middle age. 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques and tau tangles are the hallmark pathologic features of Alzheimer's disease (AD). 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the beta-amyloid precursor protein are strongly associated with some cases of familial Alzheimer's disease. 3 key findings →
Design: cross-sectional Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple biological pathways are altered and could be targeted very early in the Alzheimer's continuum. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The relationship between amyloid-β (Aβ) species and tau pathology in Alzheimer's disease (AD) is not fully understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 8,460 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.
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 30,580 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events