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Research

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

Find studies

Showing 276–300 of 317 studies published 2012 · free to read (page 12 of 13) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 317 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; 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.

Abnormal insula functional network is associated with episodic memory decline in amnestic mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 44 out of 100. NeuroImage 2012-07-06

Abnormalities of functional connectivity in the default mode network (DMN) recently have been reported in patients with amnestic mild cognitive impairment (aMCI), Alzheimer's disease (AD) or other psychiatric diseases. 4 key findings →

Evidence: low

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

The TspanC8 subgroup of tetraspanins interacts with A disintegrin and metalloprotease 10 (ADAM10) and regulates its maturation and cell surface expression

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-10-03

A disintegrin and metalloprotease 10 (ADAM10) is a ubiquitous transmembrane metalloprotease that cleaves the extracellular regions from over 40 different transmembrane target proteins, including Notch and amyloid precursor protein. 4 key findings →

Evidence: low

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

Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The American journal of pathology 2012-09-28

Lack of tau expression has been reported to protect against excitotoxicity and to prevent memory deficits in mice expressing mutant amyloid precursor protein (APP) identified in familial Alzheimer disease. 4 key findings →

Evidence: low

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

Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-04-24

Pathogenic generation of amyloid β-peptide (Aβ) by sequential cleavage of β-amyloid precursor protein (APP) by β- and γ-secretases is widely believed to causally underlie Alzheimer disease (AD). β-Secretase initially cleaves APP thereby generating a membrane-bound APP C-terminal fragment, from which γ-secretase subsequently liberates 37-43-amino acid long Aβ species. 4 key findings →

Evidence: low

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

In vivo microglia activation in very early dementia with Lewy bodies, comparison with Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Parkinsonism & related disorders 2012-07-26

Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. 4 key findings →

Evidence: low

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

Mitochondria-associated ER membranes in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular and cellular neurosciences 2012-08-24

Alzheimer disease (AD) is associated with the accumulation in the brain of extracellular neuritic plaques composed mainly of β-amyloid (Aβ) and of intracellular neurofibrillary tangles composed of hyperphosphorylated forms of the microtubule-associated protein tau. 5 key findings →

Evidence: low

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

APP mutations in the Aβ coding region are associated with abundant cerebral deposition of Aβ38

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2012-11-13

Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →

Evidence: low

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

Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Antioxidants & redox signaling 2012-02-07

Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress. 3 key findings →

Evidence: low

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

Contributions of the Framingham Heart Study to stroke and dementia epidemiologic research at 60 years

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Archives of neurology 2012-05-01

The Framingham Heart Study, the longest-running prospective epidemiologic study in history, was initiated in 1948 in response to the rising toll of coronary heart disease and hypertension. 4 key findings →

Evidence: moderate

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

Default network is not hypoactive in dementia with fluctuating cognition: an Alzheimer disease/dementia with Lewy bodies comparison

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neurobiology of aging 2012-10-11

Default mode network resting state activity in posterior cingulate cortex is abnormally reduced in Alzheimer disease (AD) patients. 2 key findings →

Evidence: low

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

Discovery of AZD3839, a potent and selective BACE1 inhibitor clinical candidate for the treatment of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2012-10-09

β-Site amyloid precursor protein cleaving enzyme1 (BACE1) is one of the key enzymes involved in the processing of the amyloid precursor protein (APP) and formation of amyloid β peptide (Aβ) species. 4 key findings →

Design: clinical trial Evidence: low

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

A G-rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurochemistry 2012-03-13

β-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the transmembrane aspartyl protease that catalyzes the first cleavage step in the proteolysis of the APP to the amyloid β-protein (Aβ), a process involved in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Montreal Cognitive Assessment (MoCA): validation study for vascular dementia

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of the International Neuropsychological Society : JINS 2012-06-08

The Montreal Cognitive Assessment (MoCA) is a brief instrument developed for the screening of milder forms of cognitive impairment, having surpassed the well-known limitations of the MMSE. 4 key findings →

Evidence: low

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

Hyperphosphorylation of Tau induced by naturally secreted amyloid-β at nanomolar concentrations is modulated by insulin-dependent Akt-GSK3β signaling pathway

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2012-08-21

Alzheimer disease (AD) is neuropathologically characterized by the formation of senile plaques from amyloid-β (Aβ) and neurofibrillary tangles composed of phosphorylated Tau. 4 key findings →

Evidence: low

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

Microglial activatory (immunoreceptor tyrosine-based activation motif)- and inhibitory (immunoreceptor tyrosine-based inhibition motif)-signaling receptors for recognition of the neuronal glycocalyx

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Glia 2012-05-21

Microglia sense intact or lesioned cells of the central nervous system (CNS) and respond accordingly. 4 key findings →

Evidence: low

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

The impact of inflammation on cognitive function in older adults: implications for healthcare practice and research

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses 2012-08-01

Accumulating evidence suggests that levels of inflammation, an immune response, increase with age throughout the body and the brain. 2 key findings →

Evidence: low

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

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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.

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