28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is pathologically characterized by a long progressive phase of neuronal changes, including accumulation of extracellular amyloid-β (Aβ) and intracellular neurofibrillary tangles, before the onset of observable symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and atherosclerosis are both chronic age- and inflammation-dependent diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Significant differences between platelet characteristics from AD patients and HC at the time of first clinical diagnosis were observed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The reliability of plasma biomarkers of Alzheimer's disease (AD) can be compromised by protease-induced degradation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Much testing in medicine is aimed at healthy people to facilitate the early detection of health conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The program would generate per-person value of $53,721 from a payer (reduction of direct cost and patient QALY gains) and $69,861 from a societal perspective (adding valuation of reduced caregiver burden). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial encephalomyopathy, lactic acidosis, and stroke (MELAS) is a mitochondrial genetic disorder caused by a point mutation, resulting in the substitution of guanine for adenine at nucleotide 3243 (A3243G). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by the gradual loss of neurons and the accumulation of amyloid plaques and neurofibrillary tangles. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The current findings implicate ADAMTS4 in both the pathological process of Aβ peptide aggregation and in the early detection of amyloid pathology in AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It can be concluded that COX-2 protein can serve as a potential blood-based biomarker for early detection and can be a good platform for therapeutic intervention for AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Given the importance of early diagnosis of AD patients, it was suggested that the measurement of plasma levels and also mRNA expression of BACE1 might be a valuable blood-based biomarker used in preference to other invasive diagnostic methods such as cerebrospinal fluid (CSF) analysis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily characterized by cognitive decline and behavioral impairments, typically manifesting in the elderly and presenile population. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In spite of having a well-resourced health system, Germany is projected to be unable to cope with the demand for biomarker-based AD diagnosis, if a disease-modifying AD treatment were introduced. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Measurements of CSF AD biomarkers show large between-laboratory variability, likely caused by factors related to analytical procedures and the analytical kits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Voxel-based morphometry (VBM) has already been applied to MRI scans of patients with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choroid plexus (CP) forming the blood-cerebrospinal fluid (B-CSF) barrier is among the least studied structures of the central nervous system (CNS) despite its clinical importance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified Abeta1-40 and Abeta1-42 in lenses from people with and without Alzheimer's disease at concentrations comparable with brain, and Abeta1-40 in primary aqueous humour at concentrations comparable with cerebrospinal fluid. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intra-blood-brain-barrier production of virus-specific antibody is good evidence of infection within the blood-brain barrier. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A number of emerging biomarkers are able to measure synapse injury and loss in the brain and may correlate with cognitive function in AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intravenous immunoglobulin (IVIg) has been proposed as a potential agent for Alzheimer's disease (AD) immunotherapy because it contains antibodies against beta-amyloid (Abeta). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is associated with the intraparenchymal growth of plaque-like amyloid deposits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
For all subjects, the greatest density of CSF-positive extracranial voxels was in the nasal turbinates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A major barrier to the effective conduct of clinical trials of new drug candidates against Alzheimer's disease (AD) and to identifying patients for receiving future disease-modifying treatments is the limited capacity of the current health system to find and diagnose patients with early AD pathology. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
There are many types of intercellular communication, and extracellular vesicles are one of the important forms of this. 1 key finding →
Evidence: low
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →