27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Atrophy in FAD is observed early, both in areas commonly associated with sporadic Alzheimer disease and also in the putamen and thalamus, 2 regions associated with early amyloid deposition in FAD mutation carriers. 4 key findings →
Design: cross-sectional Participants: 192 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau PET shows higher magnitude of binding in MAPT mutation carriers who harbor mutations that are more likely to produce AD-like tau pathology (e.g., in our series, the non-exon 10 families tend to accumulate mixed 3R/4R aggregates). 2 key findings →
Design: case-control study Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
MBs did not influence the rate of cognitive decline in patients with AD. 5 key findings →
Design: cohort study Participants: 221 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The term cerebral small vessel disease (SVD) describes a range of neuroimaging, pathological, and associated clinical features. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal analysis revealed progressive and widespread changes in the grey matter, notably including the basal ganglia. 4 key findings →
Design: cross-sectional Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to assess the agreement between data on cerebral amyloidosis, derived using Pittsburgh compound B positron emission tomography and (i) multi-laboratory INNOTEST enzyme linked immunosorbent assay derived cerebrospinal fluid concentrations of amyloid-β42; (ii) centrally measured cerebrospinal fluid amyloid-β42 using a Meso Scale Discovery enzyme linked immunosorbent assay; and (iii) cerebrospinal fluid amyloid-β42 centrally measured using an antibody-independent mass spectrometry-based reference method. 3 key findings →
Participants: 243 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our search resulted in the inclusion and full-text review of 137 articles. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The prevalence and the degree of cerebral white matter lesions increased with age. 2 key findings →
Participants: 1,077 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We report the clinical, neuroimaging, and neuropathologic features of progressive nonfluent aphasia (PNFA), a rare neurodegenerative syndrome most notable for its distinct language disturbance. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In this large cohort study of elderly subjects, the degree of dVRS appears independently associated with age, hypertension, volume of white matter hyperintensities, and lacunar infarctions. dVRS should be considered as another MRI marker of cerebral small vessel disease in the elderly with regional variations in their severity. 4 key findings →
Design: cohort study Evidence: moderate
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Cerebral white matter lesions are frequently observed on magnetic resonance imaging (MRI) scans in elderly people and are associated with stroke and dementia. 5 key findings →
Design: cross-sectional Participants: 1,625 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To accurately predict the development of Alzheimer's disease (AD) at its predementia stage would be a major breakthrough from both therapeutic and research standpoints. 5 key findings →
Design: longitudinal study Evidence: moderate
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Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time. 2 key findings →
Design: cross-sectional Evidence: moderate
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PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers. 3 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD. 4 key findings →
Design: cross-sectional Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid deposition and neurofibrillary degeneration in Alzheimer's disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer's disease pathology than others remain largely unknown. 4 key findings →
Participants: 76 Evidence: moderate
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We hypothesize that CRP (C-reactive protein) is associated with brain structural changes and may interact with amyloid to produce vascular and degenerative damage. 4 key findings →
Design: longitudinal study Participants: 736 Evidence: moderate
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The relative performance of semi-quantitative amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) markers in diagnosing Alzheimer's disease (AD) and predicting the cognitive evolution of patients with mild cognitive impairment (MCI) is still debated. 4 key findings →
Design: cross-sectional Participants: 677 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Measures are needed that identify persons that will develop Alzheimer's disease in order to target them for preventative interventions. 4 key findings →
Design: cross-sectional Participants: 20 Evidence: low
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Higher structural stiffness of the carotid artery is associated with cognitive decline, whereas both structural and load‐dependent stiffness are associated with brain structural abnormalities common in Alzheimer disease‐related dementias. 5 key findings →
Design: cohort study Participants: 2,489 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repeated subconcussive and concussive head injury. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
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To explore neural correlates of cognitive decline in aging, we used longitudinal behavioral data to identify two groups of older adults (n = 40) that differed with regard to whether their performance on tests of episodic memory remained stable or declined over a decade. 4 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer disease-specific cortical thinning and hippocampal volume loss are consistent with a sigmoidal pattern, with an acceleration phase during the early stages of the disease. 2 key findings →
Design: case-control study Participants: 317 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 2,885 studies in this tag, 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →