28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease is the most common cause of dementia in the elderly population (aged 65 years and over), followed by vascular dementia, Lewy body dementia, and rare types of neurodegenerative diseases, including frontotemporal dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta, which is strongly associated with disease progression and cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review considers the use of these mouse models in understanding the mechanisms of Aβ clearance, cerebral amyloid angiopathy (CAA), blood brain barrier breakdown, neuroinflammation, and neuronal dysfunction in response to Aβ immunotherapy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by the accumulation of amyloid-beta (Aβ) and neurofibrillary tangles of hyperphosphorylated tau in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These guidelines facilitate the accurate diagnosis and effective management of ARIA; ensure the safe administration of anti-Aβ drugs; and provide a framework for MRI facilities, includes staffing requirements and the use of MRI management systems. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of cerebral amyloid angiopathy (CAA) has been shown to increase with age, with rates reported to be around 50-60% in individuals over 80 years old who have cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Expansions of a G 4 C 2 repeat in the C9ORF72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two devastating adult-onset neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term "propagon" is used to define proteins that may transmit misfolding in vitro, in tissues or in organisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is characterized by the deposition of amyloid-β as extracellular plaques and hyperphosphorylated tau as intracellular neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases characterized by the intraneuronal accumulation of aggregated tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and associated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An 88-year-old mentally normal woman (Blessed test score = 27) had very large amounts (397/mm2) of deposits stained by anti-beta A4 serum in the first temporal gyrus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD) and other tauopathies, the cytosolic protein Tau misfolds and forms intracellular aggregates which accumulate within the brain leading to neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Considering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The development of glucagon-like peptide 1 receptor agonists (GLP-1RA) for type 2 diabetes and obesity was followed by data establishing the cardiorenal benefits of GLP-1RA in select patient populations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, including Alzheimer's Disease (AD) and Parkinson's Disease (PD) are common complications of diabetes, arising from insulin resistance, inflammation, and other pathological processes in the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We find that IRAs can cross the BBB by two separate processes; one that is fast and one that is slow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We demonstrated that TIR can ameliorate high glucose-induced neurodegeneration and overcome neuronal insulin resistance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropsychiatric symptoms are common in patients with PDD. 3 key findings →
Participants: 537 Evidence: low
Full summary, score breakdown and related studies → Original source
Recipients of galantamine 16 or 24 mg/day achieved significant improvements in cognitive and global symptoms relative to placebo recipients in large (n = 285 to 978 patients with mild to moderate AD) well-designed trials of 3 to 6 months' duration. 4 key findings →
Participants: 285 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Abeta measures increase with age, but, in contrast to reports on familial AD, plasma Abeta measures were neither sensitive nor specific for the clinical diagnosis of mild cognitive impairment or sporadic AD. 2 key findings →
Participants: 146 Evidence: low
Full summary, score breakdown and related studies → Original source
The AMPK/SIRT1/PGC-1α pathway represents a cornerstone target at the intersection of metabolism, aging, and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This single-blind, placebo controlled study reports on the effects of administering three acute doses of nicotine (0.4, 0.6 and 0.8 mg) subcutaneously to a group of Alzheimer's disease (DAT) patients (n = 22), young adult controls (n = 24), and normal aged controls (n = 24). 3 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
AimTo evaluate visual dysfunction and its correlation with structural changes in the retina in patients with Alzheimer's disease (AD).MethodsPatients with AD (n=24) and controls (n=24) underwent evaluation of visual acuity (VA), color vision (using the Farnsworth and L'Anthony desaturated (D) 15 color tests), and contrast sensitivity vision (CSV; using the Pelli-Robson chart and CSV-1000E test) to measure visual dysfunction. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
The considerable age effect requires the adaptation of cut-off values for old age. 2 key findings →
Participants: 516 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 →