Alzheimer's disease (AD) is currently the most common incurable forms of dementia. 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.
It is now generally accepted that the lesions of Alzheimer disease (AD) are associated with a host of inflammatory molecules, including complement proteins, as well as with many activated microglia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1β, IL-18) was up-regulated in severe and MILD AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The aim of this report was to describe the case of an elderly patient with cerebral amyloid angiopathy and associated dementia who presented with new onset symptomatology compatible with an acute cerebrovascular event. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging influences cerebrovascular disease expression by a variety of mechanisms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging studies link vascular risk factors and cerebrovascular health to the prevalence and rates of progression in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular risk factors and cerebrovascular disease are common causes of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic kidney disease, defined by a decreased glomerular filtration rate or albuminuria, is recognized as a major global health burden, mainly because it is an established risk factor for cardiovascular and cerebrovascular diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is cerebrovascular amyloid deposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
This research is based on the brain bank project, which combines prospective clinical follow ups and retrospective neuropathological studies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Braak's staging concept of Lewy body disease pathogenesis is based on a spatiotemporal sequence of alpha-synuclein deposition, with autonomic nervous system involvement before synucleinopathy in substantia nigra neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis is a devastating disease characterized by rapidly progressive paresis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-associated dementia (HAD) is a complication of advanced HIV disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
β-Amyloid (Aβ) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All synapses are not the same. They differ in their morphology, molecular constituents, and malleability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive decline and disease progression in different neurodegenerative diseases typically involves synaptic dysfunction preceding the neuronal loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dose-dependent decrease of Aβ40 levels in vivo confirmed suppression of BACE1 activity by both inhibitors. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ginkgo leaf is the most used form of supplement for cognitive ailments. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although intracellular accumulation of alpha-synuclein (alpha-syn) is a characteristic pathological change in Parkinson's disease, Lewy body dementia and Alzheimer's disease, the normal function of this presynaptic protein is still unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Neuronal calcium sensors (NCS) readily bind calcium and undergo conformational changes enabling them to interact and regulate specific target molecules. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapse loss and synaptic dysfunction are pathological processes already involved in the early stages of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In mature neurons, the number of synapses is determined by a neuronal activity-dependent dynamic equilibrium between positive and negative regulatory factors. 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 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 →