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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 51–75 of 125 studies published 1994 (page 3 of 5) · 27,380 in the whole library · How the 0–100 score works

Download bibliography of these 125 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; 12,859 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.

Morphologic and biochemical analysis of the intracellular trafficking of the Alzheimer beta/A4 amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1994-05-01

Abnormal metabolic processing of the beta/A4 amyloid precursor protein (APP) has been implicated in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Hippocampal sclerosis: a common pathological feature of dementia in very old (> or = 80 years of age) humans

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 1994-01-01

In a neuropathological study of 81 brains of prospectively studied subjects of 80 years of age or older at the time of death, 13 cases (16%), including 4 men and 9 women, had hippocampal sclerosis (HpScl) affecting the vulnerable region of the hippocampus. 4 key findings →

Evidence: low

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

Neuropathology and apolipoprotein E profile of aged chimpanzees: implications for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-09-01

Neuropathological findings in three aged chimpanzees were compared with those in rhesus monkeys and individuals with Alzheimer disease. 3 key findings →

Evidence: low

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

An evaluation of the predictive validity and inter-rater reliability of clinical diagnostic criteria for senile dementia of Lewy body type

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurology 1994-05-01

Several recent autopsy studies suggest that senile dementia of Lewy body type (SDLT) may be the second most common neuropathologic cause of dementia in the elderly, accounting for 7 to 30% of all cases. 1 key finding →

Evidence: low

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

Correlates of Mini-Mental Status Examination scores among elderly demented patients: the influence of race-ethnicity

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of clinical epidemiology 1994-12-01

Data on 1888 patients seen at Alzheimer's Disease Diagnostic and Treatment Centers in California were used to examine possible differences in Mini-Mental State Examination (MMSE) results for different racial-ethnic groups. 2 key findings →

Participants: 1,888 Evidence: low

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

Frequency of the apolipoprotein E epsilon 2 allele is diminished in sporadic Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neuroscience letters 1994-07-01

Recent data have demonstrated genetic disequilibrium between inheritance of the apolipoprotein E (apoE) epsilon 4 allele and increased risk of Alzheimer disease. 2 key findings →

Evidence: low

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

Conformation and fibrillogenesis of Alzheimer A beta peptides with selected substitution of charged residues

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of molecular biology 1994-11-01

A key pathological feature of Alzheimer's disease (AD) is the formation and accumulation of amyloid fibers within the neurophil as senile plaques and in the walls of cerebral and meningeal blood vessels. 4 key findings →

Evidence: low

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

The Mini-Mental State Examination score and the clinical diagnosis of dementia

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of clinical epidemiology 1994-09-01

To set a working cutoff score for the referral to diagnostic examination, we evaluated 150 consecutive patients with complaints potentially related to dementia, using the Mini-Mental State Examination (MMSE). 4 key findings →

Evidence: low

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

Human immunodeficiency virus encephalitis is the pathological correlate of dementia in acquired immunodeficiency syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Annals of neurology 1994-10-01

While dementia has been observed in approximately one-fourth of terminally ill patients with acquired immunodeficiency syndrome, it has been difficult to attribute this clinical disorder to a single neuropathological substrate. 1 key finding →

Evidence: low

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

Cell cycle-dependent regulation of the phosphorylation and metabolism of the Alzheimer amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The EMBO journal 1994-03-01

Accumulation of the amyloid A beta peptide, which is derived from a larger precursor protein (APP), and the formation of plaques, are major events believed to be involved in the etiology of Alzheimer's disease. 4 key findings →

Evidence: low

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

Chemical characterization of A beta 17-42 peptide, a component of diffuse amyloid deposits of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of biological chemistry 1994-04-01

A peptide corresponding to the amino acid sequence of A beta 17-42 (LVFFAEDVGSNKGAIIGLMVGGVVIA) was isolated from Alzheimer Disease patient brains containing large deposits of diffuse-type amyloid. 4 key findings →

Evidence: low

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

Membrane lipids, selectively diminished in Alzheimer brains, suggest synapse loss as a primary event in early-onset form (type I) and demyelination in late-onset form (type II)

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neurochemistry 1994-03-01

Major membrane lipids were quantified in frontal (Brodmann area 9) and temporal (Brodmann areas 21 and 22) cortices, caudate nucleus, hippocampus, and frontal white matter of 12 cases with Alzheimer's disease (AD) type I (early onset), 21 cases with AD type II (late onset), and 20 age-matched controls. 4 key findings →

Evidence: low

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

Secreted beta-amyloid precursor protein stimulates mitogen-activated protein kinase and enhances tau phosphorylation

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-07-01

Biological effects related to cell growth, as well as a role in the pathogenesis of Alzheimer disease, have been ascribed to the beta-amyloid precursor protein (beta-APP). 4 key findings →

Evidence: low

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

Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neuroscience 1994-09-01

The aetiology and pathogenesis of Alzheimer's disease are currently poorly understood, but symptomatic disease is associated with amyloid plaques, neurofibrillary tangles, neuronal loss and numerous alterations of neurotransmitter systems in the CNS. 4 key findings →

Evidence: low

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

S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neuroscience research 1994-11-01

Increased synthesis and release of S100 beta protein from activated astrocytes has been implicated in the overgrowth of dystrophic neurites in neuritic plaques in Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Soluble amyloid beta-protein is a marker of Alzheimer amyloid in brain but not in cerebrospinal fluid

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Biochemical and biophysical research communications 1994-05-01

The amyloid beta protein (A beta), a 4 kD fragment of the beta amyloid precursor protein, is deposited as insoluble amyloid in the brain of Alzheimer disease (AD) subjects. 4 key findings →

Evidence: low

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

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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