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Find studies

Showing 25,801–25,825 of 27,146 studies marked Peer-reviewed (page 1033 of 1086) · 28,180 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.

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.

Genetically engineered mice have been generated to model cerebral β-amyloidosis, one of the hallmarks of Alzheimer disease (AD) pathology, based on the overexpression of a mutated cDNA of the amyloid-β precursor protein (AβPP) or by knock-in of the murine Aβpp gene alone or with presenilin1 mutations. 2 key findings →

Evidence: low

Alzheimer's disease is a neurodegenerative disease in which aging is not only a major risk factor but a major determinant of onset, course, and pathogenesis. 1 key finding →

Evidence: low

The association between apolipoprotein E (apoE) and amyloid-β peptide (Aβ) may significantly impact the function of both proteins, thus affecting the etiology of Alzheimer's disease (AD). 1 key finding →

Evidence: low

Acetylcholinesterase (AChE) is now well-established widely as a signalling molecule with non-hydrolytic functions including trophic activity in a diverse variety of situations in both neural and non-neural tissues. 1 key finding →

Evidence: low

In the present work, we investigated the level of IgM autoantibodies directed against different Aβ epitopes as potential diagnostic biomarker for Alzheimer's disease (AD). 3 key findings →

Evidence: low

The present study examines N-myc and c-myc protein expression with Western blotting and single and double-labeling immunohistochemistry in the hippocampus in Alzheimer disease (AD), the striatum in Huntington disease (HD) and the substantia nigra in Parkinson disease (PD). 2 key findings →

Evidence: low

Immunocytochemistry, Western blotting, and RT-PCR were used to identify the isoforms of laminin expressed in the Alzheimer disease, but not in normal human brain tissue. 5 key findings →

Evidence: low

Alzheimer disease has been well associated with mitochondrial dysfunctions. 3 key findings →

Evidence: low

Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Neuroscience letters 1991-08-01

Brain spectrin is a major membrane skeleton protein that participates in cellular transport, cell morphogenesis, neurotransmitter release and growth cone adhesion. 3 key findings →

Evidence: low

An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). 4 key findings →

Evidence: low

Amyloid PET Ligands for Dementia

✓ Peer-reviewed alzhub usefulness score 35 out of 100. PET clinics 2010-01-01

The progressive nature of neurodegeneration suggests an age-dependent process that ultimately leads to synaptic failure and neuronal damage in cortical areas of the brain critical for memory and higher mental functions. 1 key finding →

Evidence: low

Prenatal exposure to low doses of LPS caused AD-related features including behavioral and neuropathological changes from midlife to senectitude. 2 key findings →

Evidence: low

These findings suggest that neurotrophic impairment during early development can be one of the etiopathogenic factors of AD and that the neurotrophic peptide mimetic is a potential early prevention strategy for this disease. 2 key findings →

Evidence: low

Cerebral amyloid angiopathy (CAA) is caused by the cerebrovascular deposition of Alzheimer amyloid beta protein (Abeta) and shows an increased incidence in carriers of the apolipoprotein E (APOE) epsilon4 genotype. 1 key finding →

Evidence: low

Two suggested clinical trial designs for assessing progression of Alzheimer disease are the randomized withdrawal design and the randomized start design. 3 key findings →

Evidence: high

When evaluating the 'bleeding load' with 7.0-T T₂*-weighted MRI in post-mortem brain sections of patients with dementia and vascular risk factors, only quantification of small cerebral bleeds in the cortico-subcortical regions is reliable. 3 key findings →

Evidence: low

Prevalence and pattern of major neurological disorders in rural Kashmir (India) in 1986

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Neuroepidemiology 1994-01-01

In 1986 in the Kuthar Valley in the Anantnag District of south Kashmir (northwestern India), we studied the population to ascertain the prevalence and pattern of various neurological diseases. 5 key findings →

Evidence: low

A study of emotional processing in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Brain and cognition 1998-10-01

This study investigated three aspects of processing materials with emotional content in patients with idiopathic Parkinson's disease (PD): the ability to produce affective prosody, to discriminate affectively loaded speech, and to detect the surprise element in humorous sketches. 4 key findings →

Evidence: low

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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