alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 2,826–2,850 of 8,338 studies · tagged Brain Biology (page 114 of 334) · 30,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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.

Institutions

From OpenAlex; 15,654 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.

Synaptic change in the posterior cingulate gyrus in the progression of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of Alzheimer's disease : JAD 2015-01-01

Mild cognitive impairment (MCI) is considered to be an early stage in the progression of Alzheimer's disease (AD) providing an opportunity to investigate brain pathogenesis prior to the onset of dementia. 5 key findings →

Evidence: low

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

Aβ mediates F-actin disassembly in dendritic spines leading to cognitive deficits in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-12-15

Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →

Evidence: low

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

Targeting norepinephrine in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's research & therapy 2013-04-29

Advances in AD biomarker research have demonstrated changes in amyloid-beta (Aβ), brain metabolism and other pathophysiologies prior to the onset of memory loss, with some markers possibly changing one or two decades earlier. 3 key findings →

Evidence: low

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

Rho-associated protein kinase 1 (ROCK1) is increased in Alzheimer's disease and ROCK1 depletion reduces amyloid-β levels in brain

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neurochemistry 2016-07-01

Alzheimer's disease (AD) is the leading cause of dementia and mitigating amyloid-β (Aβ) levels may serve as a rational therapeutic avenue to slow AD progression. 5 key findings →

Evidence: low

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

A novel epsilon-cleavage within the transmembrane domain of the Alzheimer amyloid precursor protein demonstrates homology with Notch processing

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Biochemistry 2002-02-01

Proteolytic processing of the transmembrane domain of the amyloid precursor protein (APP) is a key component of Alzheimer's disease pathogenesis. 4 key findings →

Evidence: low

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

Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Investigative ophthalmology & visual science 2008-06-19

Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →

Evidence: low

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

MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2008-11-05

MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR). 4 key findings →

Evidence: low

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

FMRP mediates mGluR5-dependent translation of amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 45 out of 100. PLoS biology 2007-03-01

Amyloid precursor protein (APP) facilitates synapse formation in the developing brain, while beta-amyloid (Abeta) accumulation, which is associated with Alzheimer disease, results in synaptic loss and impaired neurotransmission. 4 key findings →

Evidence: low

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

TNFalpha plus IFNgamma induce the production of Alzheimer beta-amyloid peptides and decrease the secretion of APPs

✓ Peer-reviewed alzhub usefulness score 45 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1999-01-01

The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Time course of the development of Alzheimer-like pathology in the doubly transgenic PS1+APP mouse

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Experimental neurology 2002-02-01

Doubly transgenic mice expressing both a mutated amyloid precursor protein and a mutated presenilin-1 protein accumulate A(beta) deposits as they age. 4 key findings →

Evidence: low

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

The amyloid precursor protein: a biochemical enigma in brain development, function and disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. FEBS letters 2013-05-16

For 20 years the amyloid cascade hypothesis of Alzheimer disease (AD) has placed the amyloid-β peptide (Aβ), formed from the amyloid precursor protein (APP), centre stage in the process of neurodegeneration. 4 key findings →

Evidence: low

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

{beta}-Amyloid impairs AMPA receptor trafficking and function by reducing Ca2+/calmodulin-dependent protein kinase II synaptic distribution

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2009-02-24

A fundamental feature of Alzheimer disease (AD) is the accumulation of beta-amyloid (Abeta), a peptide generated from the amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Anesthetic sevoflurane causes neurotoxicity differently in neonatal naïve and Alzheimer disease transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Anesthesiology 2010-06-01

Recent studies have suggested that children undergoing surgery under anesthesia could be at an increased risk for the development of learning disabilities, but whether anesthetics contribute to this learning disability is unclear. 4 key findings →

Evidence: low

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

Inflammatory processes induce beta-amyloid precursor protein changes in mouse brain

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-03-01

In Alzheimer disease, a combination of genetic predisposition and environmental factors may contribute to changes in beta-amyloid precursor protein (APP) expression, beta-amyloid peptide deposition, and neuronal loss. 4 key findings →

Evidence: low

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

Lysosomal proteinase antigens are prominently localized within senile plaques of Alzheimer's disease: evidence for a neuronal origin

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain research 1990-04-01

To investigate the role of proteolysis in amyloid formation, we studied the localization of the proteolytic enzymes, cathepsin D and cathepsin B, in the prefrontal cerebral cortex and hippocampus of human postmortem brains from patients with Alzheimer's disease and from individuals free of neurological disease. 4 key findings →

Evidence: low

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

Selective intracellular release of copper and zinc ions from bis(thiosemicarbazonato) complexes reduces levels of Alzheimer disease amyloid-beta peptide

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2007-12-17

Copper and zinc play important roles in Alzheimer disease pathology with recent reports describing potential therapeutics based on modulation of metal bioavailability. 4 key findings →

Evidence: low

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

Muscarinic regulation of Alzheimer's disease amyloid precursor protein secretion and amyloid beta-protein production in human neuronal NT2N cells

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1995-03-01

The Alzheimer amyloid precursor protein (APP) undergoes complex processing resulting in the production of a 4-kDa amyloid peptide (A beta) which has been implicated in the pathogenesis of Alzheimer's disease. 4 key findings →

Evidence: low

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

β-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2012-09-17

BACE1 is the β-secretase enzyme that initiates production of the β-amyloid peptide involved in Alzheimer disease. 4 key findings →

Evidence: low

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

The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2005-06-27

Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, vascular amyloid, neurofibrillary tangles, and progressive neurodegeneration. 4 key findings →

Evidence: low

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

Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1995-10-01

Phorbol esters, activators of protein kinase C (PKC), regulate the relative utilization of alternative processing pathways for the Alzheimer beta-amyloid precursor protein (beta-APP) in intact cells, increasing the production of nonamyloidogenic soluble beta-APP (s beta-APP) and decreasing that of neurotoxic beta-amyloid (A beta) peptide. 3 key findings →

Evidence: low

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

Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neuropathology and experimental neurology 2011-05-01

It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease. 4 key findings →

Evidence: low

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

Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2012-05-04

Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD). 4 key findings →

Evidence: low

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

From across this tag

10 of the 8,313 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.

↑ Change the filters

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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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