Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Corticobasal degeneration (CBD) is a neurodegenerative tauopathy-a class of disorders in which the tau protein forms insoluble inclusions in the brain-that is characterized by motor and cognitive disturbances 1-3 . 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
A role for beta-amyloid precursor protein (beta-APP) in the development of Alzheimer's disease has been indicated by genetics, and many conditions in which beta-APP is raised have been associated with an increased risk of Alzheimer's disease or an Alzheimer's-like pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Several genetic risk factors for Alzheimer's disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 . 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glymphatic movement of fluid through the brain removes metabolic waste 1-4 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The existence of human hippocampal neurogenesis has long been disputed1-12 and its relevance in cognition remains unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteolytic processing of amyloid precursor protein (APP) through an endosomal/lysosomal pathway generates carboxy-terminal polypeptides that contain an intact beta-amyloid domain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The neocortex is disproportionately expanded in human compared with mouse 1,2 , both in its total volume relative to subcortical structures and in the proportion occupied by supragranular layers composed of neurons that selectively make connections within the neocortex and with other telencephalic structures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The precise mechanisms that lead to cognitive decline in Alzheimer's disease are unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ageing is a major risk factor for many neurological pathologies, but its mechanisms remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is an incurable neurodegenerative disorder in which neuroinflammation has a critical function 1 . 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
A mutation at codon 717 of the beta-amyloid precursor protein gene has been found to cosegregate with familial Alzheimer's disease in a single family. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Innate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a common and devastating disease characterized by aggregation of the amyloid-β peptide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical outcomes of severe acute respiratory syndrome 2 (SARS-CoV-2) infection are highly heterogeneous, ranging from asymptomatic infection to lethal coronavirus disease 2019 (COVID-19). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is primarily a mouse-model study (in amyloid-plaque mouse models such as 5xFAD, with some human tissue validation) identifying a newly recognized, protective state of brain immune cells (microglia) that expresses genes normally associated with the immune system's lymphocytes. 4 key findings →
Evidence: early
Full summary, score breakdown and related studies → Original source
Mutations in the presenilin genes are the main cause of familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4 is the strongest genetic risk factor for Alzheimer's disease 1-3 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia in Alzheimer's disease progresses alongside neurodegeneration 1-4 , but the specific events that cause neuronal dysfunction and death remain poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Physical exercise is generally beneficial to all aspects of human and animal health, slowing cognitive ageing and neurodegeneration 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Macrophages are important players in the maintenance of tissue homeostasis 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immature dentate granule cells (imGCs) arising from adult hippocampal neurogenesis contribute to plasticity and unique brain functions in rodents 1,2 and are dysregulated in multiple human neurological disorders 3-5 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →