28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease is defined by the presence of β-amyloid plaques and neurofibrillary tau tangles potentially preceding clinical symptoms by many years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The default mode network (DMN) encompasses brain systems that exhibit coherent neural activity at rest. 5 key findings →
Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
Host responses to anti-amyloid-β (Aβ) antibody therapy are evident in neuroimaging changes and clinical symptoms in a subset of clinical trial subjects receiving such therapy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Unlike other aggregation inhibitors, RI-AG03 effectively suppresses aggregation of multiple Tau species containing both hotspots in vitro and in vivo, is non-toxic, and suppresses aggregation-dependent neurodegenerative and behavioral phenotypes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive reserve (CR) is defined as the ability to maintain functionality despite accumulating pathology. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
High levels of proinflammatory cytokines induce neurotoxicity and catalyze inflammation-driven neurodegeneration, but the specific release mechanisms from microglia remain elusive. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia and amyotrophic lateral sclerosis are neurodegenerative diseases with considerable clinical, genetic and pathological overlap. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite recent advances, severe acute pancreatitis (SAP) remains a lethal inflammation with limited treatment options. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Concomitant Alzheimer's disease (AD) pathology is a frequent event in the context of Lewy body disease (LBD), occurring in approximately half of all cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is widely recognized as a multifactorial disorder involving neurovascular and glial dysfunction beyond amyloid-β and tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TAR DNA-binding protein 43 (TDP-43) is an RNA binding protein found within ribonucleoprotein granules tethered to lysosomes via annexin A11. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common form of dementia; however, its molecular mechanisms are not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2) are associated with endolysosomal dysfunction across cell types, and carriers of LRRK2 mutations variably present with phosphorylated tau and α-synuclein deposits in post-mortem analysis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DLB brains show PINK1 deficiency alongside α-syn and Aβ co-pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In synucleinopathies, the protein α-synuclein misfolds into Lewy bodies (LBs) in patients with Lewy body disease (LBD) or into glial cytoplasmic inclusions (GCIs) in patients with multiple system atrophy (MSA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As an established treatment for movement disorders, deep brain stimulation (DBS) has been adapted for the treatment of Alzheimer's disease (AD) by modulating fornix activity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alpha-synuclein (α-syn) deposits are common in around half of the Alzheimer's disease (AD) cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC) refers to the aberrant accumulation of TDP-43 in the brains of ageing individuals either in isolation or in combination with neurodegenerative disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal syndrome (CBS) is associated with diverse pathological substrates such as tau, prion protein, transactive response and, rarely, alpha synuclein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rare mutations in the gene encoding presenilin2 (PSEN2) are known to cause familial Alzheimer's disease (FAD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We discovered that dendritic spine elimination-induced either artificially or in Aβ models-triggers a two-stage compensatory response: rapid enlargement of remaining spines followed by delayed spine regeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In APPL/S mice, BD10-2 treatment improved memory and LTP deficits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immunotherapies targeting extracellular tau share the premise that interrupting cell-to-cell spread of tau pathology in Alzheimer's disease (AD) will slow dementia pathogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the natural extracts tested, PanQ emerged as the most effective for increasing the active CatB isoform in correspondence with enhanced levels of synaptic proteins and the autophagy marker LC3-II. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 6,970 studies in this tag that have a study page, 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 28,580 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 →