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 30 studies in Genetics published 2006 (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other 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.

What “Genetics” covers

Genetics — Inherited risk: APOE and the other risk genes, and what they do and don't tell you.

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.

Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly. 2 key findings →

Design: cross-sectional Participants: 54 Evidence: moderate

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

Survival and mortality differences between dementia with Lewy bodies vs Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-12-01

Patients with DLB had an increased risk of mortality vs patients with AD (hazard ratio [HR] 1.88, 95% CI: 1.4 to 2.5). 3 key findings →

Design: longitudinal study Participants: 315 Evidence: moderate

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

Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →

Design: longitudinal study Participants: 1,075 Evidence: moderate

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

Conversion to dementia from mild cognitive disorder: the Cache County Study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2006-07-01

Individuals with all types of mild cognitive impairment have an elevated risk of dementia over 3 years, more so in those with an APOE epsilon4 allele. 3 key findings →

Participants: 120 Evidence: low

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

Apolipoprotein E genotype and age-related myelin breakdown in healthy individuals: implications for cognitive decline and dementia

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of general psychiatry 2006-01-01

In later-myelinating regions, the severity and rate of myelin breakdown in healthy older individuals are associated with APOE status and support the hypothesis that this process may contribute to age at onset of AD. 5 key findings →

Design: cross-sectional Participants: 104 Evidence: low

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

Brain volume changes in CADASIL: a serial MRI study in pure subcortical ischemic vascular disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2006-05-01

The NBV significantly correlated with all clinical scores (Rankin, NIH Stroke Scale, Barthel, structured interview for the diagnosis of Alzheimer dementia and multi-infarct dementia, Mattis dementia rating scale) at both time points independently of age and sex. 2 key findings →

Design: cross-sectional Evidence: low

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

The DYRK1A gene, encoded in chromosome 21 Down syndrome critical region, bridges between beta-amyloid production and tau phosphorylation in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Human molecular genetics 2006-11-29

We scanned throughout chromosome 21 to assess genetic associations with late-onset Alzheimer disease (AD) using 374 Japanese patients and 375 population-based controls, because trisomy 21 is known to be associated with early deposition of beta-amyloid (Abeta) in the brain. 4 key findings →

Evidence: low

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

Altered brain white matter integrity in healthy carriers of the APOE epsilon4 allele: a risk for AD?

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neurology 2006-04-01

Although the mechanism underlying vulnerability of white matter tracts in APOE epsilon4 carriers is still unknown, these findings suggest that increased genetic risk for developing Alzheimer disease is associated with changes in microscopic white matter integrity well before the onset of dementia. 3 key findings →

Evidence: low

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

Age and apolipoprotein E*4 allele effects on cerebrospinal fluid beta-amyloid 42 in adults with normal cognition

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Archives of neurology 2006-07-01

These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition. 2 key findings →

Evidence: low

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

24(S)-hydroxycholesterol participates in a liver X receptor-controlled pathway in astrocytes that regulates apolipoprotein E-mediated cholesterol efflux

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2006-03-08

Both apolipoprotein E (apoE) and 24(S)-hydroxycholesterol are involved in the pathogenesis of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Neurofibrillary tangle-predominant dementia: comparison with classical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Acta neuropathologica 2006-11-07

Neurofibrillary tangle predominant dementia (NFTPD) is a subset of late onset dementia, clinically different from traditional "plaque and tangle" Alzheimer disease (AD): later onset, shorter duration, less severe cognitive impairment, and almost absence of ApoE epsilon4. 1 key finding →

Evidence: low

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

The influence of Alzheimer disease family history and apolipoprotein E epsilon4 on mesial temporal lobe activation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2006-05-01

First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E epsilon4 (APOE4) are risk factors for developing AD. 1 key finding →

Evidence: low

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

Apolipoprotein E and low density lipoprotein receptor-related protein facilitate intraneuronal Abeta42 accumulation in amyloid model mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2006-09-29

The low density lipoprotein receptor-related protein (LRP) is highly expressed in the brain and has been shown to alter the metabolism of amyloid precursor protein and amyloid-beta peptide (Abeta) in vitro. 3 key findings →

Evidence: low

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

Apolipoprotein E-specific innate immune response in astrocytes from targeted replacement mice

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of neuroinflammation 2006-04-07

Here we showed that activation of primary astrocytes from TR APOE mice with LPS led to TR APOE-dependent differences in cytokine secretion that were greatest in TR APOE2 and that were associated with differences in NF-kappaB subunit activity. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

↑ 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 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