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.

Find studies

Showing 376–400 of 412 studies published 2017 · free to read (page 16 of 17) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 412 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.

Down syndrome: age-dependence of PiB binding in postmortem frontal cortex across the lifespan

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2017-03-14

Beta-amyloid (Aβ) deposition in brain accumulates as a function of age in people with Down syndrome (DS) with subsequent development into Alzheimer disease neuropathology, typically by 40 years of age. 3 key findings →

Participants: 25 Evidence: low

There are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer's disease (AD). 5 key findings →

Evidence: low

Functional correlates of TSH, fT3 and fT4 in Alzheimer disease: a F-18 FDG PET/CT study

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Scientific reports 2017-07-24

The present study was aimed to investigate the relationships between thyroid stimulating hormone (TSH), freeT3 (fT3) and freeT4 (fT4) and brain glucose consumption as detectable by means of 2-deoxy-2-(F-18) fluoro-D-glucose (F-18 FDG) Positron Emission Tomography/Computed Tomography (PET/CT) in a selected population with Alzheimer disease (AD). 4 key findings →

Participants: 87 Evidence: low

Narrative Organization Deficit in Lewy Body Disorders Is Related to Alzheimer Pathology

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in neuroscience 2017-02-08

Mildly demented LBD patients had a significant deficit judging narratives compared to non-demented patients, but this deficit was not correlated with MMSE. 4 key findings →

Participants: 30 Evidence: moderate

With a rapidly aging population, general practitioners are confronting the challenge of how to determine those who are at greatest risk for dementia and potentially need more specialized follow-up to mitigate symptoms early in its course. 4 key findings →

Evidence: low

Alzheimer's disease (AD) is a progressive, neurodegenerative brain disorder that attacks neurotransmitters, brain cells, and nerves, affecting brain functions, memory, and behaviors and then finally causing dementia on elderly people. 4 key findings →

Evidence: low

Central nervous system (CNS) inflammation and autophagy dysfunction are known to be involved in the pathology of neurodegenerative diseases. 4 key findings →

Evidence: low

Senescence accelerated mice P8 (SAMP8) show significant age-related deteriorations in memory and learning ability in accordance with early onset and rapid advancement of senescence. 4 key findings →

Evidence: low

Whilst nursing home managers recognise the potential benefits of advance care planning, barriers and challenges create a reluctance to facilitate. 3 key findings →

Participants: 178 Evidence: low

We studied the validity of longitudinal statistical inferences of clinical trials using minimization, a dynamic randomization algorithm designed to minimize treatment imbalance for prognostic factors. 1 key finding →

Design: longitudinal study Evidence: high

Small-molecule PET Tracers for Imaging Proteinopathies

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Seminars in nuclear medicine 2017-07-13

In this chapter, we provide a review of the challenges and advances in developing successful PET imaging agents for 3 major types of aggregated amyloid proteins: amyloid-beta (Aβ), tau, and alpha-synuclein (α-syn). 5 key findings →

Evidence: low

Neurotrophic factors, including the members of the neurotrophin family, play important roles in the development and maintenance of the nervous system. 1 key finding →

Evidence: low

Human stem cell models have the potential to provide platforms for phenotypic screens to identify candidate treatments and cellular pathways involved in the pathogenesis of neurodegenerative disorders. 1 key finding →

Evidence: low

Disturbance of redox homeostasis in Down Syndrome: Role of iron dysmetabolism

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Free radical biology & medicine 2017-07-10

Down Syndrome (DS) is the most common genetic form of intellectual disability that leads in the majority of cases to development of early-onset Alzheimer-like dementia (AD). 1 key finding →

Evidence: low

In CN subjects, study-wide significant (P -9 ) loci were identified for total tau near SRRM4 and C14orf79 and for hippocampal volume near MTUS1. 4 key findings →

Evidence: low

Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD). 4 key findings →

Evidence: low

Nutrition and dementia care: developing an evidence-based model for nutritional care in nursing homes

✓ Peer-reviewed alzhub usefulness score 39 out of 100. BMC geriatrics 2017-02-14

This collaboratively developed, person-centred model can support the design of new education and training tools and be readily translated into existing programmes. 2 key findings →

Evidence: low

How technology is reshaping cognitive assessment: Lessons from the Framingham Heart Study

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuropsychology 2017-11-01

Technological advances will catalyze groundbreaking discoveries for effective treatments of neurodegenerative cognitive disorders, such as AD, and inform novel strategies for dementia prevention and sustained lifelong cognitive health. 1 key finding →

Evidence: low

Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments. 5 key findings →

Evidence: low

↑ 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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