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
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 7,326–7,350 of 7,821 studies · tagged Brain Biology(page 294 of 313)· 28,980 in the whole library·How the 0–100 score works
Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)
From OpenAlex; 14,457 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.
LCN2 is not only a potential biomarker for the early diagnosis of AD but may also play a significant role in the neurodegenerative processes associated with the disease. 5 key findings →
Neuroinflammation plays a key role in Alzheimer's disease (AD), but the actions of microglial mediators may vary across stages of Aβ pathology. 1 key finding →
To the Editor: MC1 is a monoclonal anti-tau antibody developed by the Peter Davies laboratory in the 1990s to aid the neuropathological diagnosis of Alzheimer disease (AD).1 Raised against Alz-50-immunopurified paired helical filaments (PHFs) from an AD brain, MC1 recognizes a conformational, discontinuous epitope involving residues 7-9 in the N-terminus and 313-322 in the third repeat domain of tau (Figure 1A). 1 key finding →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Cell Transplantation·2026-02-01
Neurodegenerative dementias, including Alzheimer's disease and vascular dementia, have long been viewed through a neuron-centric lens. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Discover Neuroscience·2026-06-28
Flortaucipir (FTP) PET imaging was developed to quantify tau burden in tauopathies such as Alzheimer’s disease (AD) and to distinguish AD from other dementias, including frontotemporal lobar degeneration (FTLD). 4 key findings →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·MedComm·2025-03-24
In tauopathies, defects in autophagy-lysosomal protein degradation are thought to contribute to the abnormal accumulation of aggregated tau. 4 key findings →
Screening a 19,786-compound chemical diversity library, we identified > 100 compounds that corrected nuclear membrane defects in MAPT IVS10+16 neurons, with 23 demonstrating robust dose-dependent rescue. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Cerebral Cortex·2026-02-01
Von Economo neurons (VENs) are unique spindle-shaped neurons that primarily reside in the anterior cingulate (ACC) and fronto-insular (FI) cortices. 3 key findings →
Alzheimer’s disease (AD), the term “dementia”, describes a specific neuropathology together with the development and progression of age-related cognitive and functional loss. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Neurological Research·2025-07-10
Neuroinflammation, mediated by activated microglia and astrocytes, exacerbates Aβ and tau pathology, contributing to synaptic loss and neuronal death. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Frontiers in Medicine·2025-05-14
Alzheimer’s disease (AD) and related tauopathies such as frontotemporal dementia (FTD) or traumatic brain injury (TBI) are neurodegenerative disorders characterized by progressive loss of memory and cognitive function. 2 key findings →
✓ Peer-reviewedalzhub usefulness score 34 out of 100.·Small methods·2025-01-06
Spatial transcriptomics (ST) represents a revolutionary approach in molecular biology, providing unprecedented insights into the spatial organization of gene expression within tissues. 2 key findings →
✓ Peer-reviewedalzhub usefulness score 33 out of 100.·Neurobiology of aging·1996-03-01
Transgenic mice expressing the oncogenic protein-serine/threonine kinase Mos at high levels in the brain display progressive neuronal degeneration and gliosis. 2 key findings →
Our work suggests an anti-inflammatory effect of quercetin in the CA1 hippocampal region of aged triple transgenic Alzheimer's disease mice. 2 key findings →
✓ Peer-reviewedalzhub usefulness score 33 out of 100.·Neurobiology of aging·1988-03-01
Studies were undertaken to assess the extent to which messenger RNA prepared from the postmortem Alzheimer's disease (AD) brain can be used for the successful preparation of a recombinant cDNA library. 2 key findings →
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC
(62.8% of the library) and OpenAlex (17.6%),
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.
1,038 records (3.6% of the
library) are not peer-reviewed — 966 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.