30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
We report the neuropathological evaluation of a 24-year-old autistic woman suffering from a residual state of infantile autism and presenting with self-injury behavior since childhood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The segmentation application revealed ganglion cell and retinal layer atrophy in patients with AD compared with controls, especially in the inner layers of patients with long disease duration. 3 key findings →
Participants: 150 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegeneration in dementia is mainly evaluated by assessing cerebral atrophy, while retinal neurodegeneration can be quantified in vivo using optical coherence tomography (OCT). 3 key findings →
Participants: 164 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings demonstrated the macular microvascular attenuation in MCI and AD patients. 5 key findings →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with AD showed a reduced flow density in the radial peripapillary capillaries layer and in the superficial retinal OCT angiogram when compared with healthy controls. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
Retinal thickness does not discriminate EOAD from controls but is correlated to parietal cortical atrophy in both groups. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this devastating disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Machines don't have eyes, but you wouldn't know that if you followed the progression of deep learning models for accurate interpretation of medical images, such as x-rays, computed tomography (CT) and magnetic resonance imaging (MRI) scans, pathology slides, and retinal photos. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
MCI-LB is associated with neuropsychiatric symptoms and a cognitive profile similar to established DLB. 2 key findings →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source
Our aim is to review the most recent evidence on novel antibody therapies for Alzheimer's disease directed against amyloid-β. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) is essential for maintaining brain homeostasis by regulating molecular exchange between the systemic circulation and the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the amyloid β-protein (Aβ) is believed to play an initiating role in Alzheimer's disease (AD), the molecular characteristics of the key pathogenic Aβ forms are not well understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects more than 5 million Americans, with substantial consequences for individuals with AD, families, and society in terms of morbidity, mortality, and healthcare costs. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex multifaceted disease. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Currently available Alzheimer's disease (AD) therapeutics are only symptomatic, targeting cholinergic and glutamatergic neurotransmissions. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
When the US Food and Drug Administration used the accelerated approval process to authorize the use of the antiamyloid drug aducanumab to treat Alzheimer's disease (AD), many people hoped this signaled a new era of disease-modifying treatment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a diverse disease with a complex pathophysiology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study shows preliminary data on the potential combined effect of amyloid-β and tau-related pathologies on the integrity of posterior brain cortices in DLB patients, whereas only amyloid-β seems to be related to MTA. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The brain's network of perivascular channels for clearance of excess fluids and waste plays a critical role in the pathogenesis of several neurodegenerative diseases including cerebral amyloid angiopathy (CAA). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the most common dementia in the elderly, is marked by progressive cognitive decline and neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Antiamyloid therapy of Alzheimer's disease tackles the overproduction and clearance of the amyloid-beta peptide (Aβ). 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
New roles of the Renin-Angiotensin System (RAS), apart from fluid homeostasis and Blood Pressure (BP) regulation, are being progressively unveiled, since the discoveries of RAS alternative axes and local RAS in different tissues, including the brain. 2 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source
Two phase-III clinical trials with anti-amyloid peptide antibodies have met their primary goal, i.e. slowing of Alzheimer's disease (AD) progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid therapies (AATs) are increasingly being recognized as promising treatment options for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
New mouse models of AD pathologies will add to the research armamentarium, but the early models have accurately predicted responses to amyloid therapies in humans. 1 key finding →
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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