27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Acetylcholinesterase (AChE) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain acetylcholine (ACh) levels. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A conceptual model for cholinesterase inhibitors has been proposed, linking enzyme inhibition, clinical efficacy and adverse effects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rivastigmine, a carbamate inhibitor of acetylcholinesterase, is already in use for treatment of Alzheimer's disease under the trade name of Exelon. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amaryllidaceous plants produce pharmacologically active alkaloids, galanthamine being the most interesting for its use in the treatment of Alzheimer's disease as a cholinesterase inhibitor. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinesterase inhibitors have produced the best evidence of clinical efficacy for treating patients with Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycogen synthase kinase 3 (GSK-3) is a serine/threonine protein kinase that has recently emerged as a key target in drug discovery. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adenosine is a ubiquitous homeostatic substance released from most cells, including neurones and glia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results of the present study document that severe cognitive impairment may be considered a negative predictor of functional recovery after a period of intensive rehabilitation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipoprotein lipase (LPL) catalyses the hydrolysis of the triacylglycerol component of circulating chylomicrons and very low density lipoproteins, thereby providing non-esterified fatty acids and 2-monoacylglycerol for tissue utilisation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The dementia in Alzheimer disease (AD) is usually attributed to widespread neuronal loss in conjunction with the pathologic hallmarks of intracellular neurofibrillary tangles and extracellular plaques containing amyloid (A beta) in fibrillar form. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exposure to complex mixtures of air pollutants produces inflammation in the upper and lower respiratory tract. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation of alpha-synuclein has been implicated in the formation of proteinaceous inclusions in the brain (Lewy bodies, Lewy neurites) that are characteristic of neurodegenerative diseases, such as Parkinson's disease (PD) and dementia with Lewy bodies (DLBs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered dendritic spines are characteristic of traumatized or diseased brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of glial cells is to support and sustain proper neuronal function and microglia are no exception to this. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The deposition of the abundant presynaptic brain protein alpha-synuclein as fibrillary aggregates in neurons or glial cells is a hallmark lesion in a subset of neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Besides affecting the hypothalamus and other brain areas related to reproduction, ovarian steroids have widespread effects throughout the brain, on serotonin pathways, catecholaminergic neurons, and the basal forebrain cholinergic system as well as the hippocampal formation, a brain region involved in spatial and declarative memory. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Changes in hippocampal function seem critical for cognitive impairment in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein conformational disorders (PCDs), such as Alzheimer's disease, Huntington's disease (HD), Parkinson's disease and oculopharyngeal muscular dystrophy, are associated with proteins that misfold and aggregate. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta-peptide (A(beta)) is heavily deposited in the brains of Alzheimer's disease (AD) patients, and free radical oxidative stress, particularly of neuronal lipids and proteins, is extensive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approximately 30% (4115 dollars) of the total annual cost of AD (14420 dollars) is invested in the direct management of BPSD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The vitamins folic acid, B12 and B6 and B2 are the source of coenzymes which participate in one carbon metabolism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) brains display A beta (Abeta) plaques, inflammatory changes and neurofibrillary tangles (NFTs). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Drebrin, located in the dendritic spines of the neuron, plays a role in the synaptic plasticity together with actin filaments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The fluid mosaic model of the plasma membrane has evolved considerably since its original formulation 30 years ago. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 2000 the 10 leading causes of death were (in rank order) Diseases of heart; Malignant neoplasms; Cerebrovascular diseases; Chronic lower respiratory diseases; Accidents (unintentional injuries); Diabetes mellitus; Influenza and pneumonia; Alzheimer's disease; Nephritis, nephrotic syndrome and nephrosis; and Septicemia and accounted for nearly 80 percent of all deaths occurring in the United States. 4 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →