30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Well-established studies have shown an elevated level of reactive oxygen species (ROS) that induces oxidative stress in the Alzheimer's disease (AD) patient's brain and an animal model of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysfunction of microglia is known to play an important role in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An individual's genetic makeup plays a large role in determining susceptibility to Alzheimer's disease (AD) but has largely been ignored in preclinical studies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progranulin (GRN) and TMEM106B are associated with several common neurodegenerative disorders including frontotemporal lobar degeneration (FTLD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over 25 genes are known to affect the risk of developing Alzheimer disease (AD), the most common neurodegenerative dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transactive response DNA-binding protein of 43 kDa (TDP-43) functions as a heterogeneous nuclear ribonucleoprotein and is the major pathological protein in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis/motor neuron disease (ALS/MND). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite the various mechanisms that involved in the pathogenesis of Alzheimer's disease (AD), neuronal damage and synaptic dysfunction are the key events leading to cognition impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research over the years has shown that causes of Alzheimer's disease are not well understood, but over the past years, the involvement of epigenetic mechanisms in the developing memory formation either under pathological or physiological conditions has become clear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neural stem cell (NSC) reservoir can be harnessed for stem cell-based regenerative therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiplexed isobaric labeling methods, such as tandem mass tags (TMT), remarkably improve the throughput of quantitative mass spectrometry. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impairment of microglial clearance activity contributes to beta-amyloid (Aβ) pathology in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain extracellular matrix (ECM) is a highly organized system that consists of collagens, noncollagenous proteins, glycoproteins, hyaluronan, and proteoglycans. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder and represents one of the most disabling conditions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neural synchrony is intricately balanced in the normal resting brain but becomes altered in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cellular accumulation of aggregated forms of the protein tau is a defining feature of so-called tauopathies such as Alzheimer's disease, progressive supranuclear palsy, and chronic traumatic encephalopathy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau deposition is closely related to clinical presentation in atypical AD with age playing a role in determining the degree of cortical tau deposition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) can present with atypical clinical forms where the prominent domain of deficit is not memory, that is, atypical AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mouse biodistribution studies showed moderate initial brain uptake and rapid brain washout. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High levels of inflammation could be seen in amyloid-β positive MCI cases where 18 F-flortaucipir signals were low suggesting microglial activation precedes tau tangle formation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The differential diagnosis of atypical parkinsonian syndromes is challenging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
THK-5351 exhibited faster cerebellar gray matter clearance, faster cortical white matter clearance, and higher DVR estimates in AD tau-associated regions of interest than THK-5317. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The two neuropathological hallmarks of Alzheimer's disease (AD) are amyloid-[Formula: see text] plaques and neurofibrillary tangles of tau protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Medial and lateral temporal regions represent a site of significant tau accumulation in A+ subjects and possibly a useful marker of early clinical changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the diagnosis of dementia is still largely a clinical one, based on history and disease course, neuroimaging has dramatically increased our ability to accurately diagnose it. 5 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events