Cerebrospinal fluid (CSF) has become a matrix for biomarker discovery and development in recent years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
38/100
The DIAN study compared the pathophysiological markers between carriers and non-carriers of mutation for autosomal dominant Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The DIAN observational study compared the pathophysiological markers between mutation carriers and non-carriers for autosomal dominant Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Trials missing primary efficacy end points raise the question of whether the choice of drug or the limitations of disease biology were at fault. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among active and passive anti-β-amyloid (Aβ) immunotherapies for Alzheimer's disease (AD), bapineuzumab and solanezumab, two humanized monoclonal antibodies, failed to show significant clinical benefits in mild-to-moderate AD patients in large Phase III clinical trials. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, which is characterized by gradual cognitive decline associated with deterioration of daily living activities and behavioral disturbances throughout the course of the disease, is estimated to affect 27 million people around the world. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammatory cerebral amyloid angiopathy (CAA) typically affects older patients who present with acute or subacute cognitive decline, headache, behavioral change, seizures, and focal neurological deficits. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disappointing findings from recent phase III trials on amyloid-β (Aβ) immunotherapy for Alzheimer's disease (AD) have shifted the focus of such treatments to the tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Small molecular weight compounds able to inhibit formation of tau oligomers and fibrils have already been tested for Alzheimer's disease (AD) treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Glucagon-like peptide-1 (GLP-1) is derived from the processing of proglucagon in intestinal L-cells and releases insulin from pancreatic β-cells as an incretin. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A once-daily, fixed-dose combination of memantine extended-release (ER)/donepezil 28/10 mg (Namzaric™) is available in the USA for patients with moderate to severe Alzheimer's disease (AD) on stable memantine and donepezil therapy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinesterase inhibitors (ChEIs) were introduced in the therapy of Alzheimer Disease (AD) in the nineteen nineties with great expectations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dugesia tigrina is a non-parasitic platyhelminth, which has been recently utilized in pharmacological models, regarding the nervous system, as it presents a wide sensitivity to drugs. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The cholinesterase inhibitors (ChEIs) donepezil, rivastigmine and galantamine are the current mainstays in the drug treatment of Alzheimer's disease (AD). 2 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
The evidence base, although incomplete, suggests that modest treatment effect sizes are offset by risk of considerable adverse effects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The NMDA antagonist, memantine (Namenda), and the cholinesterase inhibitor, donepezil (Aricept), are currently being used widely, either individually or in combination, for treatment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is, in part, characterised by the loss of neurones in the basal forebrain cholinergic cells that project to the cerebral cortex and hippocampus. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Donepezil is the most widely used acetylcholinesterase inhibitor licensed for symptomatic treatment of mild-to-moderate Alzheimer's disease. 2 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
This standard is based on the results of large-scale, double-blind, placebo-controlled trials. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
36% of practitioners reported not having used therapies for medical conditions other than dementia in patients with AD for reasons of limited compliance in these patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common form of dementia in industrialized countries. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The combination of memantine, an N-methyl-d-aspartate (NMDA) receptor antagonist, with an acetylcholinesterase inhibitor (AChEI) is the current standard of care in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular disease (CVD), as well as secondary ischemic brain injury from cardiovascular disease, are common causes of dementia and cognitive decline in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The management of dementia in Alzheimer's disease has dramatically changed since the development of anti-dementia drugs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a disease that threatens the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
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.
- Lecanemab bei Alzheimer-Krankheit: Frühe Therapie ist sicher
- Reasons for Failed Trials of Disease-Modifying Treatments for Alzheimer Disease and Their Contribution in Recent Research
- Drug-induced cognitive impairment in the elderly
- Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders
- Second-generation anti-amyloid monoclonal antibodies for Alzheimer's disease: current landscape and future perspectives
- Acetylcholinesterase inhibitors for treating dementia symptoms - a safety evaluation
- Natural products as a rich source of tau-targeting drugs for Alzheimer's disease
- Risk factors in developing amyloid related imaging abnormalities (ARIA) and clinical implications
- Lecanemab-Associated Amyloid-β Protofibril in Cerebrospinal Fluid Correlates with Biomarkers of Neurodegeneration in Alzheimer's Disease
- Acetylcholinesterase inhibitors as disease-modifying therapies for Alzheimer's disease
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 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.
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 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 →