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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 50 studies with an author at Consejo Superior de Investigaciones Científicas (ES) (page 2 of 2) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 50 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Other institutions

From OpenAlex; 13,658 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Deficiency in the transcription factor NRF2 worsens inflammatory parameters in a mouse model with combined tauopathy and amyloidopathy

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Redox biology 2018-07-11

Chronic neuroinflammation is a hallmark of the onset and progression of brain proteinopathies such as Alzheimer disease (AD) and it is suspected to participate in the neurodegenerative process. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Alterations in cholesterol metabolism as a risk factor for developing Alzheimer's disease: Potential novel targets for treatment

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of steroid biochemistry and molecular biology 2019-03-13

Alzheimer's disease (AD) is the most common form of dementia and it is characterized by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Toward a predictive model of Alzheimer's disease progression using capillary electrophoresis-mass spectrometry metabolomics

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Analytical chemistry 2012-09-25

Alzheimer's disease (AD) is the most prevalent form of dementia with an estimated worldwide prevalence of over 30 million people, and its incidence is expected to increase dramatically with an increasing elderly population. 1 key finding →

Participants: 85 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Letters in applied microbiology 2018-04-16

Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Age-dependent accumulation of soluble amyloid beta (Abeta) oligomers reverses the neuroprotective effect of soluble amyloid precursor protein-alpha (sAPP(alpha)) by modulating phosphatidylinositol 3-kinase (PI3K)/Akt-GSK-3beta pathway in Alzheimer mouse model

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2011-04-01

Neurotrophins, activating the PI3K/Akt signaling pathway, control neuronal survival and plasticity. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Polygenic risk for white matter hyperintensities is associated with early cerebrovascular events partly through hemodynamic measures in cognitively unimpaired middle-aged and older adults with low cardiovascular risk

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in Neurology 2026-01-05

They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia. 5 key findings →

Participants: 1,072 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The American journal of pathology 2014-05-09

Disrupted cholesterol homeostasis has been reported in Alzheimer disease and is thought to contribute to disease progression by promoting amyloid β (Aβ) accumulation. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Associations of plasma SMOC1 and soluble IL6RA levels with the progression from mild cognitive impairment to dementia

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Brain, behavior, & immunity - health 2024-11-16

Despite the central role attributed to neuroinflammation in the etiology and pathobiology of Alzheimer's disease (AD), the direct link between levels of inflammatory mediators in blood and cerebrospinal fluid (CSF) compartments, as well as their potential implications for AD diagnosis and progression, remains inconclusive. 4 key findings →

Participants: 485 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Alzheimer's disease as an inflammatory disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biomolecular concepts 2017-03-01

Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The Down syndrome candidate dual-specificity tyrosine phosphorylation-regulated kinase 1A phosphorylates the neurodegeneration-related septin 4

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neuroscience 2008-10-01

The dual-specific kinase DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) is the mammalian orthologue of the Drosophila minibrain (MNB) protein kinase and executes diverse roles in neuronal development and adult brain physiology. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

STARD1 and NPC1 expression as pathological markers associated with astrogliosis in post-mortem brains from patients with Alzheimer's disease and Down syndrome

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Aging 2020-01-05

Alzheimer´s disease (AD) is a progressive neurodegenerative disorder of complex etiology, while Down syndrome (DS) is considered a genetically determined form of AD. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Regulation of inflammatory response in neural cells in vitro by thiadiazolidinones derivatives through peroxisome proliferator-activated receptor gamma activation

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2005-04-06

In most neurodegenerative disorders, including multiple sclerosis, Parkinson disease, and Alzheimer disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated astrocytes and microglia and their cytotoxic agents play a crucial pathological role. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Soluble oligomers of amyloid-β peptide disrupt membrane trafficking of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor contributing to early synapse dysfunction

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2011-06-10

β-Amyloid (Aβ), a peptide generated from the amyloid precursor protein, is widely believed to underlie the pathophysiology of Alzheimer disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Targeting CB2 receptor with a novel antagonist reverses cognitive decline, neurodegeneration and pyroptosis in a TAU-dependent frontotemporal dementia mouse model

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain Behavior and Immunity 2025-03-11

• The new CB 2 antagonist PGN36 is able to cross the Blood-Brain Barrier. • PGN36 treatment effectively alleviates TAU P301L -induced cognitive decline . • PGN36 is able to reduce TAU protein expression levels and restore synaptic plasticity. • PGN36 modulates TAU P301L -induced pyroptosis. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Pharmacological Research 2026-02-13

Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Current amyloid inhibitors: Therapeutic applications and nanomaterial-based innovations

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Progress in Neurobiology 2025-02-28

Amyloid proteins have long been in the spotlight for being involved in many degenerative diseases including Alzheimer´s, Parkinson´s or type 2 diabetes, which currently cannot be prevented and for which there is no effective treatment or cure. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The analysis of the gut microbiome during liver disease progression led to the identification of biomarkers for related mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Frontiers in Microbiology 2025-09-16

could serve as potential biomarkers for NAFLD-associated mild cognitive impairment; 3) bacterial metabolic functions involved in sugar degradation and the breakdown of tryptophan and glutamate were downregulated and linked to CXCL13 plasma levels and neuroinflammation; 4) correlations between SCFA concentrations disappeared with liver disease and cognitive impairment. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

NRF2 deficiency is associated with synaptic alterations and ether-linked phospholipid imbalance in the hippocampus

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Redox Biology 2025-08-30

Synaptic loss is a key factor in the cognitive decline observed during aging and in neurodegenerative diseases such as dementia, where synaptopathy plays a central role in hippocampal dysfunction. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Linking nutrition and aging: A cross-domain analysis of Mediterranean Diet Adhesion Screener components

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Mechanisms of Ageing and Development 2025-10-15

This study explores the scientific landscape linking the Mediterranean Diet Adherence Screener (MEDAS) to aging-related health outcomes through a comprehensive bibliometric and scoping review approach. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Relationship between Alzheimer's Disease and Type 2 Diabetes: Critical Review On Cellular and Molecular Common Pathogenic Mechanisms

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Current Alzheimer Research 2025-02-01

Both diseases exhibit common genetic, epigenetic, biochemical and physiological characteristics. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Chr21 protein-protein interactions: enrichment in products involved in intellectual disabilities, autism and Late Onset Alzheimer Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2019-12-12

Intellectual disability (ID) found in Down syndrome (DS), which is characterized by an extra copy of 234 genes on Chr21 is poorly understood. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

GCH1 genetic variation as a prognostic factor in Parkinsons disease across populations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19

BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →

Design: longitudinal study Participants: 22,825 Evidence: moderate

Full summary, score breakdown and related studies → Original source

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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 28,180 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.

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 28,180 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 →

Newest studies, as a dated timeline →    Atom feed