Various plasma biomarkers for amyloid-β (Aβ) have shown high predictability of amyloid PET positivity. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurofilament light chain (NfL) is an axonal protein that when measured in cerebrospinal fluid (CSF) serves as a biomarker of neurodegeneration. 3 key findings →
Participants: 278 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Voxel-based analyses demonstrated significant negative correlations between CSF tau and ptau(181) levels and CMRglu in the posterior cingulate, precuneus, and parahippocampal regions. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparing the discordant CSF results of each patient with the cerebral amyloid-PET results, we found that in the group with Aβ1 - 42+ and p-tau-CSF values, the amyloid-PET was positive in 51.2% and negative in 48.8% of patients, while in the group with Aβ1 - 42-and p-Tau+ CSF values, the amyloid-PET was positive in 52.6% of patients and negative in 47.4% of them. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this paper is to systematically evaluate a biased sampling issue associated with genome-wide association analysis (GWAS) of imaging phenotypes for most imaging genetic studies, including the Alzheimer's Disease Neuroimaging Initiative (ADNI). 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Apraxia of speech is a motor speech disorder characterized by combinations of slow speaking rate, abnormal prosody, distorted sound substitutions, and trial-and-error articulatory movements. 1 key finding →
Design: cross-sectional Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
18 F-MK-6240 recapitulated Braak staging and correlated with CSF tau and p-tau, normalized to Aβ42 . 18 F-MK-6240 negatively correlated with age across Braak regions in amyloid-positive participants, consistent with greater tau pathology in earlier onset AD. 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
A subset of participants received cognitive testing and/or the Movement Disorders Society Unified Parkinson's Disease Rating Scale Part III motor exam (off medication). 18F-PI-2620 uptake was low overall in Lewy body disease and correlated with β-amyloid PET in temporal lobe regions and precuneus. 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Differential FTP-PET signal patterns showed significant negative associations with domain-specific annual rates of decline. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau accumulation starts during the preclinical phase of Alzheimer's disease and is closely associated with cognitive decline. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated CSF p-tau181 and cortical 18F-PI-2620 binding was characteristic for AD while normal CSF p-tau181 with elevated subcortical 18F-PI-2620 binding was characteristic for 4RTs. 18F-PI-2620-assessed posterior cortical hypoperfusion could be used as an additional neuronal injury biomarker in AD. 5 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Data were available from 131 participants with age ranging from 65.4 to 88.2 years and mean follow up of 2.4 years (SD = 1.0). 5 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-six percent of participants were PET positive. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is one of the main hallmarks of Alzheimer's disease (AD) and two approaches are available for assessing amyloid pathology in vivo: cerebrospinal fluid (CSF) biomarkers levels and amyloid load visualized by amyloid beta positron emission tomography imaging (Amy-PET) probes. 1 key finding →
Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source
54/100
There is both clinical and neuroanatomical variability at the single-subject level in Alzheimer's disease, complicating our understanding of brain-behaviour relationships and making it challenging to develop neuroimaging biomarkers to track disease severity, progression, and response to treatment. 5 key findings →
Participants: 1,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Intergrader agreements for overall 3 × 3 mm image quality and quantitative assessment of VD and FAZ ranged between 71% and 87% (52 images). 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD) serves as an initial symptom of preclinical Alzheimer's disease (AD). 4 key findings →
Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive reserve (CR) has been introduced to explain individual differences in susceptibility to cognitive or functional impairment in the presence of age or pathology. 1 key finding →
Participants: 941 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The etiology of cerebrovascular pathology is heterogeneous. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Whereas traumatic brain injury (TBI) results in widespread disruption of neural networks, changes in regional resting-state functional connectivity patterns after insult remain unclear. 4 key findings →
Design: cross-sectional Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We observed good convergence among the 4 Good convergence was obtained among several methods for determining an optimal cutoff for 18 F-AZD4694 PET positivity. 3 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The extent to which Alzheimer neuropathology, particularly the accumulation of misfolded beta-amyloid, contributes to cognitive decline and dementia in Parkinson's disease (PD) is unresolved. 1 key finding →
Design: cross-sectional Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The combination of amyloid and tau PETs was associated with changes in management and diagnosis of MCI and dementia, and the second-generation tau PET has a strong impact on the changes in diagnosis and management in memory clinics. 5 key findings →
Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The HCTS pattern represents a definable subgroup of non-AD pathophysiology (i.e., T - [N] + ) that is associated with cognitive impairment. 2 key findings →
Participants: 684 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neither fibrillar nor nonfibrillar Aβ content alone sufficed to explain the Aβ PET findings in either AD model. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
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.
- When Is Amyloid Really Cleared? Substantial Discordance Between Centiloid Quantitation and Visual Reads of Amyloid PET after Amyloid-Targeting Therapy
- Serum albumin and beta-amyloid deposition in the human brain
- A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease
- Evaluation of dementia in the cardiovascular health cognition study
- MRI-derived brain aging trajectories across the Alzheimer's continuum: links to cognition, pathology and lifestyle risk factors
- A combination model of AD biomarkers revealed by machine learning precisely predicts Alzheimer's dementia: China Aging and Neurodegenerative Initiative (CANDI) study
- Volumetric Changes in Cerebellar Transverse Zones: Age and Sex Effects in Health and Neurological Disorders
- Cholinergic enhancement of frontal lobe activity in mild cognitive impairment
- Magnetic Resonance Images Implicate That Glymphatic Alterations Mediate Cognitive Dysfunction in Alzheimer Disease
- Association of [ 18 F]Flortaucipir–PET and Plasma p-Tau217 With Tau Neuropathology in Alzheimer Disease and Other Neurodegenerative Disorders
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →