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

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

Find studies

Showing 1–25 of 27 studies published 1996 · free to read (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

Download bibliography of these 27 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.

Depressed mood and the incidence of Alzheimer's disease in the elderly living in the community

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Archives of general psychiatry 1996-02-01

In the 852 subjects without dementia, depressed mood was more common in individuals with greater cognitive impairment. 3 key findings →

Design: longitudinal study Participants: 1,070 Evidence: moderate

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

Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1996-07-01

The entorhinal cortex (EC) plays a crucial role as a gateway connecting the neocortex and the hippocampal formation. 4 key findings →

Participants: 20 Evidence: low

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

Preclinical evidence of Alzheimer's disease in persons homozygous for the epsilon 4 allele for apolipoprotein E

✓ Peer-reviewed alzhub usefulness score 57 out of 100. The New England journal of medicine 1996-03-01

In late middle age, cognitively normal subjects who are homozygous for the epsilon 4 allele for apolipoprotein E have reduced glucose metabolism in the same regions of the brain as in patients with probable Alzheimer's disease. 3 key findings →

Evidence: low

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

The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature medicine 1996-10-01

Missense mutations in the presenilin 1 (PS1) gene cause the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated with increased levels of amyloid beta-peptides (A beta) ending at residue 42 (A beta 42) in plasma and skin fibroblast media of gene carriers. 4 key findings →

Evidence: low

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

Natural history of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) and clinical predictors of survival: a clinicopathological study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of neurology, neurosurgery, and psychiatry 1996-06-01

Onset of falls during the first year are emphasised, as they could lead to an early diagnosis and influence the prognosis of patients with PSP. 2 key findings →

Participants: 24 Evidence: low

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

Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of Disease 1996-02-01

Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein.

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

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse. 1 key finding →

Evidence: low

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

Vascular variant of prion protein cerebral amyloidosis with tau-positive neurofibrillary tangles: the phenotype of the stop codon 145 mutation in PRNP

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-01-01

Deposition of PrP amyloid in cerebral vessels in conjunction with neurofibrillary lesions is the neuropathologic hallmark of the dementia associated with a stop mutation at codon 145 of PRNP, the gene encoding the prion protein (PrP). 4 key findings →

Evidence: low

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

Evidence that the 42- and 40-amino acid forms of amyloid beta protein are generated from the beta-amyloid precursor protein by different protease activities

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

Cerebral deposition of the amyloid beta protein (A beta) is an early and invariant feature of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurobiology of aging 1996-09-01

Interleukin-1 (IL-1), an inflammatory cytokine overexpressed in the neuritic plaques of Alzheimer's disease, activates astrocytes and enhances production and processing of beta-amyloid precursor protein (beta-APP). 4 key findings →

Evidence: low

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

Tumor necrosis factor alpha inhibits glutamate uptake by primary human astrocytes. Implications for pathogenesis of HIV-1 dementia

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 1996-06-01

Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes. 4 key findings →

Evidence: low

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

Specific domains of beta-amyloid from Alzheimer plaque elicit neuron killing in human microglia

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1996-10-01

Alzheimer's disease (AD) is found to have striking brain inflammation characterized by clusters of reactive microglia that surround senile plaques. 4 key findings →

Evidence: low

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

Cognitive and neurobiologic markers of early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

Recent studies indicate that impairments in two cognitive domains characterize the cognitive abnormalities that appear earliest in the course of Alzheimer disease (AD). 2 key findings →

Evidence: low

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

Age-dependent neuronal and synaptic degeneration in mice transgenic for the C terminus of the amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1996-11-01

The molecular basis for the degeneration of neurons and the deposition of amyloid in plaques and in the cerebrovasculature in Alzheimer's disease (AD) is incompletely understood. 4 key findings →

Evidence: low

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

Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-04-01

Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis. 3 key findings →

Evidence: low

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

Gender difference in apolipoprotein E-associated risk for familial Alzheimer disease: a possible clue to the higher incidence of Alzheimer disease in women

✓ Peer-reviewed alzhub usefulness score 43 out of 100. American journal of human genetics 1996-04-01

Late-onset Alzheimer disease (AD) is associated with the apolipoprotein E (APOE)-epsilon4 allele. 5 key findings →

Participants: 58 Evidence: low

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

Relative risk of Alzheimer disease and age-at-onset distributions, based on APOE genotypes among elderly African Americans, Caucasians, and Hispanics in New York City

✓ Peer-reviewed alzhub usefulness score 43 out of 100. American journal of human genetics 1996-03-01

Apolipoprotein-E epsilon 4 (APOE-epsilon 4) has been consistently associated with Alzheimer disease (AD) and may be responsible for an earlier age at onset. 4 key findings →

Evidence: low

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

Human immunodeficiency virus type 1 infection alters chemokine beta peptide expression in human monocytes: implications for recruitment of leukocytes into brain and lymph nodes

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-01-01

Two chemokine (chemoattractant cytokines) beta peptides, macrophage inflammatory proteins 1 alpha and 1 beta (MIP-1 alpha and MIP-1 beta), were induced in human monocyte cultures following infection with the human immunodeficiency virus type 1 (HIV-1). 4 key findings →

Evidence: low

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

Prevalence of dementia in an elderly rural population: effects of age, sex, and education

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurology, neurosurgery, and psychiatry 1996-06-01

In both Alzheimer and vascular dementia subtypes, the prevalence rates did not differ between men and women, but increased with age and were higher in subjects with a low level of education. 2 key findings →

Evidence: low

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

Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-02-01

As in Alzheimer-disease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751 mRNA. 4 key findings →

Evidence: low

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

Psychiatric morbidity in terminally ill cancer patients. A prospective study

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Cancer 1996-09-01

In the study by Derogatis et al., which included patients with all stages of cancer, 47% of the patients met the DSM-III criteria for a psychiatric disorder, with adjustment disorders being the most common. 4 key findings →

Participants: 26 Evidence: low

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

Cognitive test performance in a community-based nondemented elderly sample in rural India: the Indo-U.S. Cross-National Dementia Epidemiology Study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. International psychogeriatrics 1996-01-01

Interpretation of cognitive test performance among individuals from a given population requires an understanding of cognitive norms in that population. 5 key findings →

Evidence: low

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

↑ 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.

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