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 Helpline800-272-390024 hours a day, 365 days a yearFree, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
988 Suicide & Crisis Lifeline98824/7Call 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) Helpline866-232-84849:00 am - 9:00 pm ET, seven days a weekLicensed 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 101–125 of 317 studies published 2001(page 5 of 13)· 27,380 in the whole library·How the 0–100 score works
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.
Gene targeting of the adaptor molecule DAP12 in mice caused abnormal distribution and impaired antigen presentation capacity of dendritic cells (DCs). 4 key findings →
✓ Peer-reviewedalzhub usefulness score 52 out of 100.·Annals of neurology·2001-06-01
Several mutations in the amyloid precursor protein (APP) gene have been found to associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels. 4 key findings →
This study provides a potential standardized definition for frailty in community-dwelling older adults and offers concurrent and predictive validity for the definition.
Our objective was to examine whether rapid eye movement (REM) sleep behavior disorder occurs in disproportionally greater frequency in multiple system atrophy (MSA), Parkinson's disease (PD), and dementia with Lewy bodies (DLB), collectively known as the synucleinopathies, compared to other nonsynucleinopathy neurodegenerative disorders. 5 key findings →
We propose the following sequence of events in the development of neuropathologic changes of Alzheimer disease in Down syndrome: (1) intracellular accumulation of Abeta in neurons and astrocytes, (2) deposition of extracellular Abeta and formation of diffuse plaques, and (3) development of neuritic plaques and neurofibrillary tangles with activation of microglial cells. 1 key finding →
The findings confirm predictions regarding behavioural differences in frontotemporal and semantic dementia and point to differential roles of the frontal and temporal lobes in affect, social functioning, eating, and compulsive behaviour. 2 key findings →
The development of novel treatments for Alzheimer's disease (AD), aimed at ameliorating symptoms and modifying disease processes, increases the need for early diagnosis. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 50 out of 100.·Neurology·2001-09-01
These are the first AD incidence rates to be reported from the Indian subcontinent, and they appear to be among the lowest ever reported. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 50 out of 100.·Biochemistry·2001-07-01
Fibrillar alpha-synuclein is a component of the Lewy body, the characteristic neuronal inclusion of the Parkinson's disease (PD) brain. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 50 out of 100.·Radiology·2001-04-01
Hippocampal ADC was significantly different between control subjects and MCI patients, many of whom likely have preclinical Alzheimer disease. 2 key findings →
People with dementia or delirium have increased mortality in the 6 months after hip fracture, but depression might take longer to have an effect. 2 key findings →
Cross-sectional positron emission tomography (PET) studies find that cognitively normal carriers of the apolipoprotein E (APOE) epsilon4 allele, a common Alzheimer's susceptibility gene, have abnormally low measurements of the cerebral metabolic rate for glucose (CMRgl) in the same regions as patients with Alzheimer's dementia. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 50 out of 100.·PubMed Central·2001-09-01
The TIV normalization of cross-sectional brain volumes significantly reduced interindividual variation; the coefficient of variation (CV) was reduced from 10.0% to 6.0% in controls (P <.001). 5 key findings →
The authors performed a 6-week, randomized, double-blind, placebo-controlled, parallel-group trial of carbamazepine (400 mg/day) with 21 agitated subjects (16 completers) who had been treated unsuccessfully with antipsychotics. 1 key finding →
Screening caregivers for burden and depression and designing interventions to decrease the consequences of behavioral disturbance on caregivers would be relevant avenues to explore to decrease institutionalization of people with dementia. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 48 out of 100.·Acta neuropathologica·2001-11-28
Study of the hippocampal formation of 82 subjects, including 25 control subjects from 33 to 83 years of age, 34 subjects with Alzheimer disease (AD) from 65 to 89 years of age, and 23 subjects with Down syndrome (DS) from 33 to 72 years of age, revealed hippocampal vasculopathy with fibrosis and calcification (VFC) in 40% of control, 59% of AD, and 4% of DS subjects. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 48 out of 100.·Neurology·2001-03-01
Proton MR spectroscopy (MRS) studies have found both decreased N-acetylaspartate (NAA) and increased myo-inositol in the occipital, temporal, parietal, and frontal regions of patients with AD, even at the early stages of the disease. 1 key finding →
Progressive atrophy was revealed in presymptomatic individuals, with posterior cingulate and neocortical temporoparietal cortical losses, and medial temporal-lobe atrophy. 1 key finding →
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 tierup to 10 pts
Journal's citation recordup to 4 pts
Study designup to 12 pts
Strength of evidenceup to 5 pts
Peer-review validationup to 10 pts
How recentup to 5 pts
Sample sizeup to 4 pts
Effect reportedup to 3 pts
Studied in peopleup to 3 pts
Randomised / blindedup to 2 pts
Times citedup to 7 pts
Citations per yearup to 5 pts
Impact for its field and yearup to 6 pts
Cited by studies hereup to 6 pts
Still being citedup to 4 pts
Senior author's track recordup to 4 pts
Institution's track recordup to 3 pts
Multi-centre collaborationup to 3 pts
Indexed in PubMedup to 2 pts
Free to readup 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.