30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In contrast, tau tracer AV-1451 is reported to bind to specific types of tau fibrils (in particular to AD-associated and CTE) with higher binding affinity and only show nonspecific or weaker binding toward tau fibrils dominant with 3R isoforms (associated with PiD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of β-amyloid (Aβ) and tau, and subcortical vascular cognitive impairment (SVCI) is characterized by cerebral small vessel disease (CSVD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support a protective role for TSPO ligands in tauopathy, reducing neuroinflammation, neurodegeneration, and brain atrophy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Depression is one of the common psychiatric disorders in old age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study supports the use of noninvasive [11C]PiB PET in the assessment of Abeta deposition in the brain. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer's disease (AD). 1 key finding →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
The extracellular buildup of amyloid beta (Aβ) plaques in the brain is a hallmark of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
However, the observed spatial extent of amyloid-β exceeds these tightly circumscribed areas, suggesting that previous studies may have underestimated the negative impact of amyloid-β on intrinsic connectivity. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Having a parent affected with late-onset Alzheimer's disease (LOAD) is a major risk factor among cognitively normal (NL) individuals. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
This study revealed that prefrontal Aβ deposition correlates with apathy. 3 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
Testosterone and gonadotropins have been associated with cognitive decline in men and the modulation of β amyloid (Aβ) metabolism. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
The major genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is a C9orf72 G 4 C 2 repeat expansion 1,2 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In early Alzheimer's disease (AD), the hippocampal region is the area most severely affected by cellular and structural alterations, yet glucose hypometabolism predominates in the posterior association cortex and posterior cingulate gyrus. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The PERK-eIF2α branch of the Unfolded Protein Response (UPR) mediates the transient shutdown of translation in response to rising levels of misfolded proteins in the endoplasmic reticulum. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The volume of parcellated cortical regions is a composite measure related to both thickness and surface area. 2 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
It is typically associated with frontal lobe atrophy, although patterns of atrophy are heterogeneous. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
In AD, the observed patterns of WM abnormalities may reflect the advanced phase of a secondary degenerative process and an association, especially in the early phases of the disease, with primary WM tract damage over and above GM abnormalities. 3 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings support the notion that age at onset modulates the distribution of cortical involvement, and that disproportionate precuneus atrophy is more prominent in patients with a younger age of onset. 5 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
The duration and sequence of EEG microstates reflect specific aberrations of frontal lobe functions in FTD and schizophrenia. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Marked grey matter atrophy occurs in PD with dementia but far less extensive changes are evident in PD-MCI. 2 key findings →
Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source
Functional magnetic resonance imaging (fMRI) of default mode network (DMN) brain activity during resting is recently gaining attention as a potential noninvasive biomarker to diagnose incipient Alzheimer's disease. 1 key finding →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
How hexanucleotide GGGGCC (G 4 C 2 ) repeat expansions in C9orf72 cause frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is not understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This Alzheimer's Association workgroup paper proposes a major update to how Alzheimer's disease is diagnosed: it defines the disease by biological markers (amyloid plaques and tau tangles detected via blood, CSF, or PET) rather than requiring clinical symptoms like memory loss to be present. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
This review article discusses the FDA's May 2025 clearance of Fujirebio's Lumipulse G blood test, the first FDA-cleared blood test for aiding Alzheimer's diagnosis (via the pTau217/beta-amyloid 1-42 ratio). 4 key findings →
Evidence: moderate
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 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.
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 →