28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the aducanumab-treated mice, we identified 17 significantly regulated proteins that were associated with 1) mitochondria and metabolism (ACAT2, ATP5J, ETFA, EXOG, HK1, NDUFA4, NDUFS7, PLCB1, PPP2R4), 2) cytoskeleton and axons (ADD1, CAPZB, DPYSL3, MAG), 3) stress response (HIST1H1C/HIST1H1D, HSPA12A), and 4) AβPP trafficking/processing (CD81, GDI2). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with early symptomatic Alzheimer's disease showed less cognitive and functional decline with donanemab compared with placebo in a Phase 2 study offering up to 72 weeks of treatment. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The US FDA approved Aducanumab in June 2021 as the first Alzheimer's disease (AD) drug under its accelerated approval pathway. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
On 7 June , the FDA approved aducanumab, the first new drug for Alzheimer’s disease in almost 20 years—and notably, the first drug with a putative disease‐modifying mechanism for the treatment of this devastating disorder, namely the removal of β‐amyloid (or Aβ) plaques from the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is the most common form of dementia with global burden projected to triple by 2050. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab has recently been licensed by the Food and Drug Administration (FDA) in the USA under its ‘accelerated approval’ pathway (to provide earlier access to treatments that fulfil an unmet need based on a surrogate endpoint) for treatment of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
En junio, la Agencia de Alimentos y medicamentos de los Estados Unidos (FDA) otorgó aprobación mediante vía acelerada al medicamento aducanumab, desarrollado por Biogen, Inc. para tratamiento de la enfermedad de Alzheimer (EA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab is a human immunoglobulin G1 anti‐amyloid beta (Aβ) antibody currently being evaluated for potential treatment of patients with early Alzheimer’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the approval of aducanumab on the “Accelerated Approval Pathway” and the recognition of amyloid load as a surrogate marker, new successful therapeutic approaches will be driven by combination therapy as was the case in oncology after the launch of immune checkpoint inhibitors. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab, a human monoclonal antibody, was approved in June of 2021 as the first disease-modifying treatment for Alzheimer’s disease by the United States Food and Drug Administration (U.S. FDA). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is a major cause of morbidity and mortality. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Three new drugs are presented: dostarlimab, loncastuximab tesirine, and aducanumab. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
EEG characteristics that correlate with the cognitive functions are important in detecting mild cognitive impairment (MCI) in T2DM. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological conditions such as epilepsy cause misregulation of adult neural stem/progenitor populations in the adult hippocampus in mice, and the resulting abnormal neurogenesis leads to impairment in learning and memory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates intracellular levels of PIP3 and antagonizes the PI3K signaling pathway important for cell survival. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous studies of human hepatic encephalopathy (HE) have shown decreased levels of glial fibrillary acidic protein (GFAP) in Alzheimer type II astrocytes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of liver failure, characterized neuropathologically by astrocyte swelling, microglial activation and Alzheimer Type II astrocytosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Basal ganglia, cerebral cortex and subcortical white matter were studied for glial fibrillary acidic protein (GFAP) in four cases of hepatic encephalopathy (HE) with Alzheimer II gliosis and five age-matched controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Previous studies have described altered expression of metallothioneins (MTs) in neurodegenerative diseases like multiple sclerosis (MS), Down syndrome, and Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Both (18)F-FDG and (11)C-PiB imaging appear to be of limited use for predicting the progression from MCI to dementia due to AD in short-term follow-up, irrespective of the strategy of analysis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Inexpensive, non-invasive tools for assessing Alzheimer-type pathophysiologies are needed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to compare brain glial fibrillary acidic protein (GFAP) levels to the modifications of cognitive functions (Blessed test score [BTS]), the density of the main neuropathological lesions (senile plaques [SP] and neurofibrillary tangles [NFT]), and the density of the two main subtypes of beta A4 deposits (classic plaques and diffuse deposits) in a series of patients with normal aging and senile dementia of the Alzheimer type of various degrees of severity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The GFAP mRNA levels were compared to the density of the senile plaques (SP) in postmortem brain samples of 8 cases, either non-demented or affected by senile dementia of the Alzheimer type. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →