28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The use of positive modulators of PLA2 (especially of cPLA2 and iPLA2) or supplementation with dietary lipid compounds (e.g., arachidonic acid) in combination with cognitive training could be a valuable therapeutic strategy for cognitive enhancement in early-stage AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, the most common cause of dementia, has a high global economic impact. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It has been suggested that the physical basis for dementia is structural or functional loss of synapses. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dopamine loss in the substantia nigra causes several of the motor signs seen in Parkinson's disease, but there is now increasing evidence highlighting the importance of cholinergic loss in the pathophysiology of nonmotor symptoms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
N-Terminally truncated and pyroglutamate (pGlu) modified amyloid beta (Abeta) peptides are major constituents of amyloid deposits in sporadic and inherited Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid formation is a key pathological feature of Alzheimer's disease and is considered to be a major contributing factor to neurodegeneration and clinical dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium and dementia share similarities in clinical and pathogenic features, leading to the speculation that instead of being distinct clinical entities, the two age-related conditions may be linked by a common pathogenic mechanism. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium is a profound, acute confusional state that leads to long-term cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These preliminary study results show an association between human brain activity of microglia, astrocytes, and IL-6 and delirium in elderly patients and add to the accumulating evidence that inflammatory mechanisms are involved in delirium. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TDP-43 proteinopathies are characterized by loss of nuclear TDP-43 and accumulation of the protein in the cytosol as ubiquitinated protein aggregates. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium is a common and severe neuropsychiatric syndrome characterised by acute deterioration and fluctuations in mental status. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is widely accepted that inflammation plays some role in the progression of chronic neurodegenerative diseases such as AD (Alzheimer's disease), but its precise role remains elusive. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A large percentage of patients subjected to general anesthesia at 65 years and older exhibit postoperative delirium (POD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) represents the interface between the brain and other body tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Systemic inflammatory events often precipitate acute cognitive dysfunction in elderly and demented populations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The demonstration that isoflurane contributes to well-described mechanisms of Alzheimer's neuropathogenesis provides a plausible link between the acute effects of anesthesia, a well-described risk factor for delirium, and the more long-term sequelae of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that synaptic dysfunction is a key pathophysiological hallmark in neurodegenerative disorders, including Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent intriguing reports have shown an association between major depression and selective and persistent loss of hippocampal volume, prompting considerable speculation as to its underlying causes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Smaller hippocampal volume is reported in major depressive disorder (MDD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation and adiposity might relate to cognitive decline via influences on brain morphology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A dysregulated hypothalamic-pituitary-adrenal axis (HPA) has been implicated in major depressive disorder and most commonly used animal models of depression have been shown to elevate circulating levels of plasma corticosterone. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Acute stress suppresses new cell birth in the hippocampus in several species. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic restraint stress (CRS) induces the remodeling (i.e., retraction and simplification) of the apical dendrites of hippocampal CA3 pyramidal neurons in rats, suggesting that intrahippocampal connectivity can be affected by a prolonged stressful challenge. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 7,799 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.
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 28,980 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 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 →