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.

The frontotemporal dementia-motor neuron disease continuum

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Lancet (London, England) 2016-03-14

Early reports of cognitive and behavioural deficits in motor neuron disease might have been overlooked initially, but the concept of a frontotemporal dementia-motor neuron disease continuum has emerged during the past decade. 5 key findings →

Evidence: low

Factor analysis showed four robust and meaningful symptom clusters: factor 1-stereotypic and eating behaviour; factor 2-executive dysfunction and self care; factor 3-mood changes; factor 4-loss of social awareness. 4 key findings →

Participants: 33 Evidence: low

A key aspect of social cognition is the ability to infer other people's mental states, thoughts and feelings; referred to as 'theory of mind' (ToM). 2 key findings →

Participants: 12 Evidence: low

Differentiating frontal and temporal variant frontotemporal dementia from Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 2000-06-01

The double dissociation in performance on semantic memory and attention/executive function clearly separated the temporal and frontal variants of FTD and aids the early differentiation of FTD from AD. 3 key findings →

Evidence: low

Disinhibition is a common behavioural symptom in frontotemporal dementia but its neural correlates are still debated. 3 key findings →

Participants: 14 Evidence: low

This multimodal approach enhanced the system's performance and provided a clinically informative method for neuroimaging analysis. 1 key finding →

Participants: 44 Evidence: low

Behavioural-variant frontotemporal dementia: diagnosis, clinical staging, and management

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Lancet. Neurology 2010-12-10

Patients with behavioural-variant frontotemporal dementia (bvFTD) present with insidious changes in personality and interpersonal conduct that indicate progressive disintegration of the neural circuits involved in social cognition, emotion regulation, motivation, and decision making. 5 key findings →

Evidence: low

Neuroinflammation in frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature reviews. Neurology 2019-07-19

Frontotemporal dementia (FTD) refers to a group of progressive neurodegenerative disorders with different pathological signatures, genetic variability and complex disease mechanisms, for which no effective treatments exist. 4 key findings →

Evidence: low

Executive function in progressive and nonprogressive behavioral variant frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurology 2008-11-01

Contrary to some prior reports, behavioral variant frontotemporal dementia (bv-FTD) patients who progress over time are typically impaired on executive tasks at first presentation, although an important minority of true FTD patients perform normally. 3 key findings →

Evidence: low

This study provides pathological validation that the new criteria assist with separating PPA cases with AD pathology into the new lv-PPA syndrome and found that a number of diagnostic clinical features (disinhibition, food preferences and naming) did not assist in discriminating the different FTD syndromes. 2 key findings →

Evidence: low

Differentiation of logopenic (lvPPA) and nonfluent/agrammatic (nfvPPA) variants of Primary Progressive Aphasia is important yet remains challenging since it hinges on expert based evaluation of speech and language production. 3 key findings →

Evidence: low

Both patient groups performed equally poorly on tests of episodic and semantic memory with the exception of immediate and delayed story recall, which was worse in the AD group. 4 key findings →

Evidence: low

Progressive and non-progressive patients are difficult to differentiate on the basis of current clinical diagnostic criteria for FTD but a combination of general cognitive, executive dysfunction and impaired ADL measures appear to be the most promising discriminators. 2 key findings →

Participants: 71 Evidence: low

Eating behavior in frontotemporal dementia: Peripheral hormones vs hypothalamic pathology

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurology 2015-09-16

In bvFTD, they are in part related to hypothalamic degeneration, with potential disintegration of the network connections between the hypothalamus and orbitofrontal cortex/reward pathways. 1 key finding →

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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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