Chronic inflammation in the brain is found in a range of neurodegenerative diseases such as Parkinson's or Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Chronic inflammation in the brain is found in a range of neurodegenerative diseases such as Parkinson's or Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this mini-review/opinion article we describe evidence that multiple cellular and molecular alterations in Alzheimer's disease (AD) pathogenesis involve perturbed cellular calcium regulation, and that alterations in synaptic calcium handling may be early and pivotal events in the disease process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (7-36)--amide (GLP-1) is an endogenous insulinotropic peptide that is secreted from the gastrointestinal tract in response to food. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive and degenerative disorder accompanied by cognitive impairment, but effective strategies against AD are currently not available. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes mellitus has been identified as a risk factor for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β protein (Aβ) is considered to be partly responsible for the impairment of learning and memory in Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Incretins are a group of gastrointestinal hormones detected both peripherally and in the central nervous system (CNS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (GLP-1) is an endogenous intestinal peptide that enhances glucose-stimulated insulin secretion. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The incretins glucagon-like peptide 1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP) are growth factors with neuroprotective properties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Analogues of the incretins Glucagon-like peptide 1 (GLP-1) and Glucose-dependent insulinotropic peptide (GIP) have been developed to treat type 2 diabetes mellitus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results indicated that subcutaneous administration of liraglutide restores both peripheral and brain insulin sensitivity and ameliorates tau hyperphosphorylation in rats with type 2 diabetes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this study was to investigate the effect of liraglutide on Alzheimer-like learning and memory impairment in mice, which were intracerebroventricularly (i.c.v.) injected with streptozotocin (STZ). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is a global problem reaching near epidemic numbers that manifests clinically with cognitive problems that decades later may result in dementias like Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an endogenous 30-amino acid gut peptide, which binds at the GLP-1 receptor coupled to the cyclic AMP second messenger pathway. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In recent years, VIP/PACAP/secretin family has special interest. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, it has been shown that in patients with AD (Alzheimer's disease) and, to some degree, in patients with PD (Parkinson's disease) insulin signalling is impaired. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The biomarker profile for AD among Mexican American cases is significantly different from that previously identified among non-Hispanic cases from many large-scale studies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild traumatic brain injury (mTBI) represents a major and increasing public health concern and is both the most frequent cause of mortality and disability in young adults and a chief cause of morbidity in the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an insulinotropic hormone, secreted from the enteroendocrine L cells of the intestinal tract in response to nutrient ingestion. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The link between diabetes mellitus and Alzheimer's disease (AD) has been known for the last few decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes has been identified as a risk factor for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
G protein-coupled receptors (GPCRs) play pivotal roles in regulating the function and plasticity of neuronal circuits in the nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the human presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Owing to improving preventative, diagnostic, and therapeutic measures for cardiovascular disease and a variety of cancers, the average ages of North Americans and Europeans continue to rise. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucose-dependent insulinotropic polypeptide (GIP) is a member of the incretin hormones and growth factors. 1 key finding →
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events