28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Harmine, a β-carboline alkaloid, is a high affinity inhibitor of the dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this article, we first present a summary of the general assumptions about Down syndrome (DS) still to be found in the literature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta protein (Abeta) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of Abeta40 and Abeta42(43), respectively. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We show that the glutathione pools in hepatic cells and in the blood are quite insensitive to fluctuations in amino acid input and offer an explanation based on model predictions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intracellular protein trafficking plays an important role in neuronal function and survival. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Huntington's disease is a progressive, fatal, neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, which encodes an abnormally long polyglutamine repeat in the huntingtin protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research into the heterogeneous nature of cognitive impairment documented in patients with Parkinson's disease (PD) has focused on disentangling deficits that vary between individuals, evolve and respond differentially to pharmacological treatments, and relate differentially to PD dementia (PDD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
By identifying aggregation-prone segments in proteins, AGGRESCAN http://bioinf.uab.es/aggrescan/ shall facilitate (i) the identification of possible therapeutic targets for anti-depositional strategies in conformational diseases and (ii) the anticipation of aggregation phenomena during storage or recombinant production of bioactive polypeptides or polypeptide sets. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Higher spontaneous production of interleukin 1 or tumor necrosis factor alpha by peripheral blood mononuclear cells may be a marker of future risk of Alzheimer disease (AD) in older individuals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is caused by the build-up of amyloid beta (A$\beta$) proteins in the brain, leading to memory loss and cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein aggregation is a hallmark of neurodegenerative diseases, including Alzheimer's disease, making the development of anti-aggregation therapeutics a critical area of research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adult hippocampal neurogenesis declines with aging and in neurological disorders, leading to cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) play crucial roles in neuronal development, synaptic transmission, and neuroplasticity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The elevated level of cerebrospinal fluid (CSF) Tau and phosphorylated Tau181 (p-Tau181) proteins are well established hallmarks of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is suggested to be involved in several neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic brain ischemia is a prominent risk factor for neurological dysfunction and progression for dementias, including Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurotoxic effects of amyloid β peptides are mediated through deregulation of intracellular Ca(2+) homeostasis and signaling, but relatively little is known about amyloid β modulation of Ca(2+) homeostasis and its pathological influence on glia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by loss of memory and cognitive abilities, and the appearance of amyloid plaques composed of the amyloid-β peptide (Aβ) and neurofibrillary tangles formed of tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The excitotoxin quinolinic acid (QUIN) is synthesized through the kynurenine pathway (KP) by activated monocyte lineage cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular cognitive impairment is the second most common form of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the loss of cognitive functions, reflecting pathological damage to the medial prefrontal cortex (mPFC) as well as to the hippocampus and the entorhinal cortex. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE), particularly the e4 allele, is genetically linked to the incidence of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intranasal insulin administration raises central nervous system (CNS) insulin levels in humans and acutely facilitates verbal memory in patients with Alzheimer's disease (AD), an effect that may differ by APOE genotype. 2 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 →