Neurodegenerative diseases pose a substantial socioeconomic burden on society. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative diseases pose a substantial socioeconomic burden on society. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the median age of the population increases, the number of individuals with Alzheimer's disease (AD) and the associated socio-economic burden are predicted to worsen. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia substantially increases lifetime costs of care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The MBI-C provides the first measure specifically developed to assess the MBI construct as explicitly described in the criteria. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive change affecting patients after anaesthesia and surgery has been recognised for more than 100 yr. Research into cognitive change after anaesthesia and surgery accelerated in the 1980s when multiple studies utilised detailed neuropsychological testing for assessment of cognitive change after cardiac surgery. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroimaging-based single subject prediction of brain disorders has gained increasing attention in recent years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overall, the application of ML to mental health has demonstrated a range of benefits across the areas of diagnosis, treatment and support, research, and clinical administration. 4 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
The genetics dataset yielded two subtypes of AD characterized mainly by the presence/absence of the apolipoprotein E (APOE) ε4 genotype, but also involving differential presence of risk alleles of CD2AP, SPON1 and LOC39095 SNPs that were associated with differences in the respective patterns of brain atrophy, especially in the precuneus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accurate diagnosis of Alzheimer's disease (AD) and its early stage, i.e., mild cognitive impairment, is essential for timely treatment and possible delay of AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We developed a comprehensive set of quality indicators of appropriate and inappropriate end-of-life care in people with Alzheimer's disease, cancer or chronic obstructive pulmonary disease, to be used in population-level research. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The early motor manifestations of sporadic amyotrophic lateral sclerosis (ALS), while rarely documented, reflect failure of adaptive complex motor skills. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
S100B is a Ca 2+ -binding protein mainly concentrated in astrocytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized neuropathologically by neuronal cell loss, extracellular neuritic plaques composed of β-amyloid (Aβ), and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Direct measurements of lysosomal pH uncovered a significant elevation (0.6 units) as a basis for slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be unstable or less active when lysosomal pH is persistently elevated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) have an increased risk of early-onset Alzheimer's Disease (AD), largely owing to a triplication of the APP gene, located on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The dosage of the serine threonine kinase DYRK1A is critical in the central nervous system (CNS) during development and aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although dementia has been described in ancient texts over many centuries (e.g., "Be kind to your father, even if his mind fail him." - Old Testament: Sirach 3:12), our knowledge of its underlying causes is little more than a century old. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The new CPS provides a functional view of cognitive performance, using readily available MDS data. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) of the amyloid-beta (Abeta) type is the most common form of sporadic CAA and is now also accepted as an early and integral part of Alzheimer's disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ratio of the longer (i.e., Aβ42/Aβ43) to shorter (i.e. Aβ40) species is a critical factor determining amyloid fibril formation, neurotoxicity and progression of the amyloid pathology in Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aberrant cleavage of amyloid precursor protein (APP) by γ-secretase contributes to the development of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Angiotensin II receptor blockers (ARBs) are widely prescribed for the medication of systemic hypertension and congestive heart failure. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Deposition of the amyloid beta-peptide (Abeta) is a pathophysiological event associated with Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) refers to the specific deposition of amyloid fibrils in the leptomeningeal and cerebral blood vessel walls, often causing secondary vascular degenerative changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent paradigm shift towards a more biologically oriented definition of Alzheimer's disease (AD) in clinical settings increases the need for sensitive biomarkers that can be applied in population-based settings. 5 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 →