28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral atrophy has been detected in patients with Parkinson's disease (PD) both with and without dementia, however differentiation based on genetic status has thus far not yielded robust findings. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Relying on procedural memory is a promising approach for interventions that address the cognitive difficulties found in semantic dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Real-World Implementation, Deployment, and Validation of Early Detection Tools and Lifestyle Enhancement (AD-RIDDLE) project, recently launched with the support of the EU Innovative Health Initiative (IHI) public-private partnership and UK Research and Innovation (UKRI), aims to develop, test, and deploy a modular toolbox platform that can reduce existing barriers to the timely detection, and therapeutic approaches in Alzheimer's disease (AD), thus accelerating AD innovation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent failures of potential novel therapeutics for Alzheimer's disease (AD) have prompted a drive towards clinical studies in prodromal or preclinical states. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Attentional fluctuations over 20-40 seconds assessed in daily life, are sensitive to clinical status and genetic risk for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The digitalized complex figure test evaluated copying performance quantitatively and further elucidated the patients' ongoing process during copying. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiday BRANCH is a feasible, reliable, and valid cognitive measure that may be useful for identifying subtle changes in learning and memory processes in older adults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with impaired clearance of β-amyloid (Aβ) from the brain, a process normally facilitated by apolipoprotein E (apoE). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
One of the major neuropathological findings in the brains of individuals with Alzheimer's disease (AD) is a loss of synaptic contacts in both the neocortex and hippocampus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gene expression profiles of more than 10,000 individual microglial cells isolated from cortex and hippocampus of male and female App NL-G-F mice over time demonstrate that progressive amyloid-β accumulation accelerates two main activated microglia states that are also present during normal aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E4 (apoE4), one of the three common isoforms of apoE, has been implicated in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Raising insulin acutely in the periphery and in brain improves verbal memory. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study provides empirical support for the suggestion that the APOE locus is the major susceptibility gene for late-onset AD in the human genome, with an OR significantly greater than any other locus in the human genome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genes play a strong role in Alzheimer's disease (AD), with late-onset AD showing heritability of 58-79% and early-onset AD showing over 90%. 2 key findings →
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
Aging is the strongest risk factor for Alzheimer's disease (AD), although the underlying mechanisms remain unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal intranuclear inclusion disease (NIID) is a slowly progressing neurodegenerative disease characterized by eosinophilic intranuclear inclusions in the nervous system and multiple visceral organs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipids play a more significant role in Parkinson's disease and its related brain disorders than is currently recognized, supporting a "lipid cascade". 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The syndrome of hypogonadotropic hypogonadism, ataxia, and dementia can be caused by inactivating mutations in RNF216 or by the combination of mutations in RNF216 and OTUD4. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data for the first time provide evidence of potential causal links between gut microbiome and AD, MDD, and SCZ. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Molecular defects in this gene have been causally associated with Kufor-Rakeb syndrome (#606693), an autosomal recessive form of juvenile-onset parkinsonism, and neuronal ceroid lipofuscinosis (#606693), a neurodegenerative disorder characterized by the intracellular accumulation of autofluorescent lipopigments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aetiological and clinical heterogeneity is increasingly recognized as a common characteristic of Alzheimer's disease and related dementias. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are resident immune cells in the central nervous system (CNS) that originate from myeloid progenitor cells in the embryonic yolk sac and are maintained independently of circulating monocytes throughout life. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Signalling through the receptor protein Notch, which is involved in crucial cell-fate decisions during development, requires ligand-induced cleavage of Notch. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Point mutations in the presenilin-1 gene (PS1) are a major cause of familial Alzheimer's disease. 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 →