28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The prevalence of cerebral amyloid angiopathy (CAA) has been shown to increase with age, with rates reported to be around 50-60% in individuals over 80 years old who have cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term "propagon" is used to define proteins that may transmit misfolding in vitro, in tissues or in organisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD) and other tauopathies, the cytosolic protein Tau misfolds and forms intracellular aggregates which accumulate within the brain leading to neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Considering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, including Alzheimer's Disease (AD) and Parkinson's Disease (PD) are common complications of diabetes, arising from insulin resistance, inflammation, and other pathological processes in the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We find that IRAs can cross the BBB by two separate processes; one that is fast and one that is slow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recipients of galantamine 16 or 24 mg/day achieved significant improvements in cognitive and global symptoms relative to placebo recipients in large (n = 285 to 978 patients with mild to moderate AD) well-designed trials of 3 to 6 months' duration. 4 key findings →
Participants: 285 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Abeta measures increase with age, but, in contrast to reports on familial AD, plasma Abeta measures were neither sensitive nor specific for the clinical diagnosis of mild cognitive impairment or sporadic AD. 2 key findings →
Participants: 146 Evidence: low
Full summary, score breakdown and related studies → Original source
The AMPK/SIRT1/PGC-1α pathway represents a cornerstone target at the intersection of metabolism, aging, and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A group of European experts was commissioned by the European Chapter of the International Federation of Clinical Neurophysiology to gather knowledge about the state of the art of the therapeutic use of transcranial direct current stimulation (tDCS) from studies published up until September 2016, regarding pain, Parkinson's disease, other movement disorders, motor stroke, poststroke aphasia, multiple sclerosis, epilepsy, consciousness disorders, Alzheimer's disease, tinnitus, depression, schizophrenia, and craving/addiction. 5 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source
The adult quiescent blood-brain barrier (BBB), a structure organised by endothelial cells through interactions with pericytes, astrocytes, neurons and microglia in the neurovascular unit, is highly regulated but fragile at the same time. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a fatal progressive neurodegenerative disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple EHR components provide a more consistent and higher performance than a single one for the selected phenotypes. 5 key findings →
Participants: 175 Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease is a recognisable clinical syndrome with a range of causes and clinical presentations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In 2025, several major advances have marked the field of neurology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab is an anti-amyloid monoclonal antibody, recently approved in the UK as a treatment for mild cognitive impairment (MCI) and mild dementia due to Alzheimer's disease (AD) in adults who are apolipoprotein E ε4 gene (APOE4) heterozygotes or non-carriers.A group of UK neurologists, old age psychiatrists and geriatricians with expertise in AD convened to agree appropriate use recommendations for lecanemab in UK clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, the U.S. Food and Drug Administration (FDA) approved 2 anti-amyloid monoclonal antibodies, aducanumab (June 7, 2021) and lecanemab (July 6, 2023), for the treatment of Alzheimer's disease (AD) patients, and will most likely also approve a 3rd one, donanemab, soon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the recent approval by the FDA of the first disease-modifying drug for Alzheimer's Disease (AD), personalized medicine will be increasingly important for appropriate management and counseling of patients with AD and those at risk. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hardy and Mummery discuss the recent positive findings in the clinical trial of lecanemab in early Alzheimer’s disease, and the implications for the amyloid hypothesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundLecanemab and donanemab are anti-amyloid-β monoclonal antibodies recently approved in the United States and Europe for the treatment of early Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Out of 538 articles, 23 (4.27%) were published in journals from the geriatric category, 44 (8.18%) included an author affiliated with a geriatric institution. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The calibrated model predicts that endogenous plaque turnover is slow, with an estimated half-life of 2.75 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent advent of anti-amyloid-β monoclonal antibodies has introduced new demands for MRI-based screening of amyloid-related imaging abnormalities, particularly the hemorrhage subtype (ARIA-H). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, the leading cause of dementia, is defined by extracellular amyloid‑β (Aβ) plaques, intracellular tau aggregates and neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,071 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 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 →