28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Androstene derivatives incorporating amino acid methyl esters were prepared, and their anti‐inflammatory effects were evaluated in lipopolysaccharide (LPS)‐activated BV‐2 microglial cells. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia serve key homeostatic roles, and respond to neuronal perturbation and decline with a high spatiotemporal resolution. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial activation has been widely demonstrated to mediate inflammatory processes that are crucial in several neurodegenerative disorders. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently available therapies for adult onset neurodegenerative diseases provide symptomatic relief but do not modify disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Agitation is not only a frequent and disturbing behavior for many patients with dementia, but it also troubles their caregivers and families. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Food and Drug Administration–approved information and public advertisements belie neurodegenerative risks for second-generation antipsychotics in affective illness. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mortality rates alone are no longer a sufficient guide to quality of care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropsychiatric symptoms of Alzheimer’s disease (NPS-AD) are highly prevalent and lead to poor medical and functional outcomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found a significantly greater intensity of cytoplasmic immunostaining for HDAC4 and HDAC6 in granule cells of the dentate gyrus in cases of FTLD overall compared with controls, and specifically in cases of FTLD tau‐ P icks compared with FTLD tau‐ MAPT and controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Three Newcastle patients bearing an expansion in C9ORF72 were identified. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
How does the brain maintain to-be-remembered information in working memory (WM), particularly when the focus of attention is drawn to processing other information? 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MoCA is suited for the cognitive screening of patients with small vessel disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cellular studies suggest sphingolipids may cause or accelerate amyloid-beta (Aβ) and tau pathology but in vivo human studies are lacking. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is the first study to report ISF Aβ and tau levels in the human brain without significant brain injury. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disturbed homocysteine metabolism is a risk factor for Alzheimer's disease (AD) and may contribute to the disease pathophysiology by increasing both amyloid-beta (Abeta) production and phosphorylated tau (P-tau) accumulation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found GSK3B gene variants associated with cognitive function and CSF biomarkers T-tau and Aβ42. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to elucidate the natural history of senile myoclonic epilepsy, a type of myoclonic epilepsy associated with Alzheimer's disease in adult Down syndrome patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies in vitro have suggested that acetylcholinesterase (AChE) may interact with beta-amyloid to promote deposition of amyloid plaques in the brain of patients with Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated tau expression has been proposed as a possible basis for impaired axonal transport in Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease neuropathology is characterised by beta-amyloid plaques and neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have isolated two recombinant cDNAs whose corresponding RNAs have an increased abundance in scrapie-infected hamster brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease that affects neurons and glial cells and leads to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cannabinoid type 2 (CB(2)) agonists are neuroprotective and appear to play modulatory roles in neurodegenerative processes in Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and experimental evidence point to a possible role of cerebrovascular dysfunction in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →