27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Four biomarkers of neuronal protein oxidation [W/S ratio of MAL-6 spin-labeled synaptosomes, phenylhydrazine-reactive protein carbonyl content, glutamine synthetase (GS) activity, creatine kinase (CK) activity] in three brain regions [cerebellum, inferior parietal lobule (IPL), and hippocampus (HIP)] of Alzheimer's disease (AD)-demented and age-matched control subjects were assessed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal accumulation of the presynaptic protein alpha-synuclein has recently been implicated in the pathogenesis of Alzheimer's and Parkinson's diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress markers as well as high concentrations of copper are found in the vicinity of Abeta amyloid deposits in Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Curcumin is the major yellow pigment extracted from turmeric, a commonly used spice in Asian cuisine and extensively employed in ayurvedic herbal remedies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apart from the damago to ascending cholinergic projections in Alzheimer's disease, biochemical studies on human brain post mortem have revealed a number of other neurochemical abnormalities. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glutamate transporters are involved in the maintenance of synaptic glutamate concentrations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Markers of serotonin synapses in entire temporal lobe and frontal and temporal neocortex were examined for changes in Alzheimer's disease by use of both neurosurgical and autopsy samples. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Deposits of amyloid beta-peptide (A beta), reduced glucose uptake into brain cells, oxidative damage to cellular proteins and lipids, and excitotoxic mechanisms have all been suggested to play roles in the neurodegenerative process in Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The problem of the etiology of Alzheimer's disease has not been solved. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial oxidative stress is a key pathologic factor in neurodegenerative diseases, including Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The transcription factor NF-kappaB is expressed in neurons wherein it is activated in response to a variety of stress- and injury-related stimuli including exposure to cytokines such as tumor necrosis factor-alpha (TNFalpha), and excitotoxic and oxidative insults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering members of the DR family by death ligands results in the transduction of either apoptotic or survival signals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The evidence is compelling that free radicals, plus increases in free cytosolic Ca2+ and Na+, figure prominently in neuronal death after exposure to glutamate and dicarboxylic excitotoxins such as NMDA and kainate. 2 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
Emerging evidence highlights the central role of peripheral immune-metabolic regulation in the pathogenesis of Alzheimer's disease and related dementias (ADRD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are neurodegenerative diseases characterized by the accumulation of misfolded tau protein and include Alzheimer's disease (AD) and related dementia disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic cerebral hypoperfusion (CCH) profoundly affects patient well-being and has been proposed as a risk factor for cognitive impairment and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The different Alzheimer and Pick tau folds establish the existence of molecular conformers of assembled tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence transcends the traditional central nervous system (CNS)-centric perspective, revealing that neutrophils, red blood cells (RBCs), and platelets may play critical roles in AD pathogenesis by modulating systemic inflammatory responses, disrupting blood-brain barrier integrity, and participating in the CNS-peripheral interactions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In tauopathies, defects in autophagy-lysosomal protein degradation are thought to contribute to the abnormal accumulation of aggregated tau. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Screening a 19,786-compound chemical diversity library, we identified > 100 compounds that corrected nuclear membrane defects in MAPT IVS10+16 neurons, with 23 demonstrating robust dose-dependent rescue. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Von Economo neurons (VENs) are unique spindle-shaped neurons that primarily reside in the anterior cingulate (ACC) and fronto-insular (FI) cortices. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD), the term “dementia”, describes a specific neuropathology together with the development and progression of age-related cognitive and functional loss. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The PS19 mouse model expressing the P301S tau mutation exhibits tau pathology associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation, mediated by activated microglia and astrocytes, exacerbates Aβ and tau pathology, contributing to synaptic loss and neuronal death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 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.
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 →