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

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.

Prevalence, characteristics, and survival of frontotemporal lobar degeneration syndromes

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neurology 2016-04-01

Key features of this study include the revised diagnostic criteria with improved specificity and sensitivity, an unrestricted age range, and simultaneous assessment of multiple FTLD syndromes. 3 key findings →

Evidence: low

Focal cortical presentations of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Brain : a journal of neurology 2007-10-01

To determine the frequency of Alzheimer's disease (AD) pathology in patients presenting with progressive focal cortical syndromes, notably posterior cortical atrophy (PCA), corticobasal syndrome (CBS), behavioural variant frontotemporal dementia (bvFTD), progressive non-fluent aphasia (PNFA) (or a mixed aphasia) and semantic dementia (SD); and to compare the age of onset, evolution and prognosis in patients with focal cortical presentations of AD versus more typical AD and those with non AD pathology. 1 key finding →

Participants: 200 Evidence: low

What the left and right anterior fusiform gyri tell us about semantic memory

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2010-10-15

The study of patients with semantic dementia, a variant of frontotemporal lobar degeneration, has emerged over the last two decades as an important lesion model for studying human semantic memory. 4 key findings →

Participants: 21 Evidence: moderate

The cortical anatomy of 6 patients with semantic dementia (the temporal lobe variant of frontotemporal dementia) was contrasted with that of a group of age-matched normal subjects by using voxel-based morphometry, a technique that identifies changes in gray matter volume on a voxel-by-voxel basis. 4 key findings →

Evidence: low

This study investigated cross-sectional and longitudinal neuropsychological data from 55 patients: 38 with Alzheimer's disease and 18 with mild cognitive impairment (MCI). 1 key finding →

Design: cross-sectional Participants: 55 Evidence: moderate

Mr M, a patient with semantic dementia--a neurodegenerative disease that is characterized by the gradual deterioration of semantic memory--was being driven through the countryside to visit a friend and was able to remind his wife where to turn along the not-recently-travelled route. 2 key findings →

Evidence: low

The rise and fall of frequency and imageability: noun and verb production in semantic dementia

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Brain and language 2000-06-01

This study examines the impact of progressive degeneration of conceptual knowledge on the content words used in connected speech elicited using the Cookie Theft picture description (Goodglass & Kaplan. 1983). 3 key findings →

Design: cross-sectional Evidence: moderate

Progressive non-fluent aphasia (PNFA) is a syndrome in which patients lose the ability to communicate fluently in the context of relative preservation of single word comprehension and non-linguistic cognitive abilities. 4 key findings →

Evidence: low

Two patients with nonfluent progressive aphasia, who have been studied longitudinally, are contrasted with a group of 5 patients with fluent progressive aphasia or semantic dementia. 5 key findings →

Evidence: low

Phonological and articulatory impairment in Alzheimer's disease: a case series

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain and language 2000-11-01

We demonstrate that phonological and articulatory impairments may occur at presentation or early in the course of Alzheimer's disease, contrary to claims that these aspects of language production are relatively preserved until the final stages of this disease. 1 key finding →

Evidence: low

It has been claimed that semantic dementia (SD), the temporal variant of fronto-temporal dementia, is characterized by an across-the-board deficit affecting all types of conceptual knowledge. 2 key findings →

Evidence: low

In order to explore the impact of a degraded semantic system on the structure of language production, we analysed transcripts from autobiographical memory interviews to identify naturally-occurring speech errors by eight patients with semantic dementia (SD) and eight age-matched normal speakers. 2 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 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