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
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
A new family of multitarget molecules able to interact with acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), as well as with monoamino oxidase (MAO) A and B, has been synthesized. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The therapeutic approach for improving the cognitive function in patients with Alzheimer's disease (AD) is mainly based on the potentiation of central cholinergic activity and is achieved clinically by the use of acetylcholinesterase (AChE) inhibitors such as tacrine, donepezil, rivastigmine, galantamine and other drugs currently in clinical trials. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing attention is being paid to inappropriate medication use in nursing homes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipid-mediated signalling regulates a plethora of physiological processes, including crucial aspects of brain function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Psychotropic drugs acting on monoamine neurotransmission are major pharmacological treatments for neuropsychiatric conditions such as schizophrenia, depression, bipolar disorder, Tourette syndrome, ADHD, and Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Hyperphosphorylated tau plays an important role in the formation of neurofibrillary tangles in brains of patients with Alzheimer's disease (AD) and related tauopathies and is a crucial factor in the pathogenesis of these disorders. 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
Epidemiological, clinical and experimental evidence suggests a link between type 2 diabetes and Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycogen synthase kinase3 (GSK3) is emerging as a prominent drug target in the CNS. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Hyperphosphorylation of the microtubule-associated protein tau is a characteristic feature of neurodegenerative tauopathies including Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent epidemiological evidence suggests that some antihypertensive medications may reduce the risk for Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lithium is a well-established therapeutic option for the acute and long-term management of bipolar disorder and major depression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disease worldwide. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent advances in cellular and molecular biology have resulted in the identification of two novel, hitherto completely unexpected targets of lithium's actions, discoveries that may have a major impact on the future use of this unique cation in biology and medicine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trials report that the class of drugs known as statins may be neuroprotective in Alzheimer's and Parkinson's disease, and further trials are currently underway to test whether these drugs are also beneficial in multiple sclerosis and acute stroke treatment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hypothesis that amyloid-beta (Abeta) peptides are the primary cause of Alzheimer's disease (AD) remains the best supported theory of AD pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The deposition of beta-amyloid peptide (A beta), the hyperphosphorylation of tau protein and the death of neurons in certain brain regions are characteristic features of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A wide range of agents and conditions are known to disrupt the ability of the endoplasmic reticulum (ER) to fold proteins properly, resulting in the onset of ER dysfunction/stress. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings demonstrate that alpha-1 adrenoceptor stimulation in the PFC impairs cognitive function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the past several years, we postulated that the loss of Wnt signaling was implicated in the pathology of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lithium has been used clinically to treat bipolar disorder for over half a century, and remains a fundamental pharmacological therapy for patients with this illness. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Low serum vitamin B12 levels are associated with neurodegenerative disease and cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycogen synthase kinase 3 (GSK-3) is a major kinase implicated in the pathogenesis of Alzheimer's disease (AD), and reducing its activity may have therapeutic efficacy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is second only to Alzheimer's disease as the most common devastating human neurodegenerative disorder. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,475 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease
- Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodent
- Safety and efficacy of pimavanserin in patients with Lewy body dementia experiencing dementia-related psychosis in the HARMONY study
- In vivo imaging of tau pathology using multi-parametric quantitative MRI
- A randomised, double-blind, placebo-controlled crossover trial on cannabinoid-based medication for behavioural disorders in old patients with severe dementia: the study results
- Insomnia in Older Adults
- Adverse outcomes associated with inappropriate drug use in nursing homes
- The 2017 hormone therapy position statement of The North American Menopause Society
- Neurodegenerative diseases: From available treatments to prospective herbal therapy
- The role of GLP-1 in neuronal activity and neurodegeneration
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,980 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →