Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Analysis of the genotyping data revealed that the TMEM106B locus consists of four major haplotypes: HA/Ha (covering the coding region), and HB/Hb (covering the upstream regulatory region). 5 key findings →
Participants: 182 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.036), with lower scores in PCA and lvPPA (median 21 and 21, respectively) compared with CBS-AD (median 27). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The most common clinical symptoms in FTLD-TDP-PSP were memory loss (100%) followed by parkinsonism (80%), early falls (60%), and behavioral variant FTD (60%). 5 key findings →
Participants: 270 Evidence: low
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We compare patterns of gray matter loss on MRI in subjects presenting as corticobasal syndrome (CBS) with Alzheimer disease pathology (CBS-AD) to those presenting as CBS with corticobasal degeneration pathology (CBS-CBD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid PET enables improved detection of amyloid-β plaques within the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lewy body dementia (LBD), which includes dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), is characterized by cognitive decline, sleep disturbances, motor dysfunction, and other debilitating clinical symptoms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
DLB with rapid cognitive decline showed greater CA1 αSYN oligomer burden (p = 0.029) and tau burden (p = 0.029) than DLB with slow decline. 5 key findings →
Evidence: low
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This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
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Overexpression of Alzheimer amyloid precursor protein (APP) produces dramatically different phenotypes in transgenic mice depending on the genetic background. 1 key finding →
Evidence: low
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Typical normative models appear appropriate for remote self‐administered measures and are sensitive to cognitive impairment. 3 key findings →
Participants: 167 Evidence: low
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Area under the receiver operating characteristic curves differentiating PSP and controls were improved by PC1 subtraction in the frontal white matter (0.54 to 0.67; P = 0.002) and subcortical (0.69 to 0.87; P < 0.001) regions. 4 key findings →
Participants: 141 Evidence: moderate
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Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We tested association of nine late-onset Alzheimer's disease (LOAD) risk variants from genome-wide association studies (GWAS) with memory and progression to mild cognitive impairment (MCI) or LOAD (MCI/LOAD) in older Caucasians, cognitively normal at baseline and longitudinally evaluated at Mayo Clinic Rochester and Jacksonville (n>2000). 5 key findings →
Evidence: low
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172 patients with symptomatic prion disease were identified. 165 (94.8%) patients experienced ≥1 symptom/sign likely to benefit from palliative care, yet only 113 (65.7%) patients accessed palliative care resources during the illness course (hospice care: 39.7%; palliative care consultation: 14.9% inpatient, 6.9% outpatient; both: 3.4%). 5 key findings →
Participants: 172 Evidence: low
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We describe a right-handed man who developed progressive nonfluent aphasia and apraxia of speech beginning at age 71. 2 key findings →
Evidence: low
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The table shows a comparative analysis stratified by young-onset AD (YOAD, onset <65 years) and late-onset AD (LOAD, onset ≥65 years). 5 key findings →
Participants: 75 Evidence: moderate
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Cotton wool plaques (CWP) are large, ball-like plaques lacking dense amyloid cores that displace adjacent structures. 3 key findings →
Evidence: low
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Genetic analyses showed that the triggering receptor expressed in myeloid cells 2 (TREM2) p.R47H variant increases the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The C9orf72 hexanucleotide repeat expansion mutation is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, but its cell type-specific effects on energy metabolism and immune pathways remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Deregulation of amyloid precursor protein (APP) processing with increased production of amyloid beta-peptide (Abeta) is considered to be a key pathogenic event in Alzheimer's disease (AD). 4 key findings →
Design: clinical trial Evidence: low
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Autoimmune encephalitis (AE) is a potentially treatable cause of rapidly progressive dementia that may mimic Creutzfeldt-Jakob disease (CJD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) and Down syndrome (DS) brains contain deposits of amyloid-beta peptide that are located extracellularly in the neuropil and in blood vessels walls. 2 key findings →
Evidence: low
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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 28,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →