28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Patients receiving chronic corticosteroid therapy have smaller hippocampal volumes, lower N-acetyl aspartate ratios, and declarative memory deficits compared with controls. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Six patients with Hashimoto thyroiditis (HT) and associated encephalopathy (HE) are described and compared with 14 well-documented cases retrieved from the literature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An accurate and early diagnosis of Alzheimer's disease (AD) is important to select optimal patient care and is critical in current clinical trials targeting core AD neuropathological features. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hippocampus is important for memory formation and is severely affected in the brain with Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complement system plays critical roles in development, homeostasis, and regeneration in the central nervous system (CNS) throughout life; however, complement dysregulation in the CNS can lead to damage and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gene ontology analyses coupled with bioinformatics approaches revealed drug targets and transcriptional regulators of microglial modules predicted to favorably modulate neuroinflammation in AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Senolytics are a class of drugs that selectively clear senescent cells (SC). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is the second most common degenerative disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current technological advancements in clinical and research settings have permitted a more intensive and comprehensive understanding of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The majority of putative disease-modifying treatments in development for Alzheimer's disease are directed against the amyloid-β (Aβ) peptide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab, a human-derived antibody targeting amyloid-β (Aβ), is in Phase 3 clinical trials for the treatment of Alzheimer's disease. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Since its discovery in 1984, the beta amyloid peptide has treaded the boards of neurosciences as the star molecule in Alzheimer's disease pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Development of disease-modifying treatments for Alzheimer's disease (AD) has been challenging, with no drugs approved to date. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a neurodegenerative disorder mainly characterized by β-amyloid deposit and tau hyperphosphorylation with no curative treatments. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are conventionally demarcated as disorders with selective loss of neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive accumulation of misfolded amyloid proteins in intracellular and extracellular spaces is one of the principal reasons for synaptic damage and impairment of neuronal communication in several neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review summarizes and describes the use of curcumin in diagnosis, prevention, and treatment of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is associated with cerebral accumulation of amyloid-β peptide and hyperphosphorylated tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a debilitating neurodegenerative disease that causes a progressive decline in memory, language and problem solving. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein misfolding into amyloid fibrils is linked to more than 40 as yet incurable cell- and neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, an eversible, progressive disease that causes problems with memory, thinking, language, planning, and behavior. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a growing global health concern with a massive impact on affected individuals and society. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Curli amyloid fibrils secreted by Enterobacteriaceae mediate host cell adhesion and contribute to biofilm formation, thereby promoting bacterial resistance to environmental stressors. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Three monoclonal antibodies directed against specific forms of the amyloid-β (Aβ) peptide have been granted accelerated or traditional approval by the FDA as treatments for Alzheimer disease, representing the first step towards bringing disease-modifying treatments for this disease into clinical practice. 3 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 →