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.

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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.

Cerebellar degeneration associated with human immunodeficiency virus infection

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurology 1998-01-01

Cerebellar disorders associated with HIV infection are typically the result of discrete cerebellar lesions resulting from opportunistic infections such as toxoplasmosis and progressive multifocal leukoencephalopathy or primary CNS lymphoma. 2 key findings →

Evidence: low

The past decade has shed new light on the etiology of Alzheimer's disease (AD), which is the consequence of interactions between numerous lesions. 1 key finding →

Evidence: low

Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Frontiers in cellular neuroscience 2020-08-13

Age-related chronic inflammatory activation of microglia and their dysfunction are observed in many neurodegenerative diseases, and the potential contributions of these dysfunctional cells to neurodegeneration have been demonstrated recently. 4 key findings →

Evidence: low

Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with acquired immune deficiency syndrome. 4 key findings →

Evidence: low

Higher teacher‐student ratio was associated with greater gray matter volume (β = 6.25, 95% CI: 1.57, 10.92) but was not associated hippocampal volume (β = ‐0.01, 95% CI: ‐0.14, 0.11), ventricular volume (β = ‐0.04, 95% CI: ‐0.13, 0.04), or white matter hyperintensity (β = ‐0.02, 95% CI: ‐0.31, 0.26) (Table 2). 5 key findings →

Participants: 450 Evidence: moderate

Linear regression models showed that higher community deprivation on the ADI was associated with greater WMH volume, independently of age, sex, years of education, smoking, and time between study visits (beta=0.11, p =.028). 4 key findings →

Participants: 388 Evidence: low

We identified 13 meaningful resting-state networks, and the dFNC among them derived four states exhibiting different connection patterns. 5 key findings →

Participants: 19 Evidence: low

Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), Neuropsychiatric Inventory Questionnaire (NPI-Q), and Clinical Dementia Rating (CDR) scale plus National Alzheimer's Coordinating Center-Frontotemporal Lobar Degeneration module (NACC-FTLD). 5 key findings →

Participants: 168 Evidence: low

Compared with stage 0 CKM syndrome, stages 3 and 4 were significantly associated with an increased risk of dementia (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.14-1.59; HR, 1.80; 95% CI 1.57-2.07). 5 key findings →

Participants: 389,287 Evidence: low

Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. 2 key findings →

Evidence: low

Recent advancements in molecular biomarkers and therapeutic options for Alzheimer's disease have brought into focus the need for greater progress in the second most common cause of dementia, vascular cognitive impairment and dementia (VCID). 5 key findings →

Evidence: low

• Anterior cingulate cortex (ACC) hypometabolism is a non-specific finding in many brain disorders. • ACC hypometabolism was more common in vascular cognitive impairment and dementia (VCID) than Alzheimer dementia (AD). • ACC hypometabolism correlated with cerebral small vessel disease markers. • ACC hypometabolism may be associated with motor stereotypies in VCID. • FDG-PET patterns of hypometabolism may identify vascular contributions to cognitive impairment The anterior cingulate cortex (ACC) is an important hub in the executive and salience networks. 2 key findings →

Participants: 379 Evidence: moderate

variants) was not associated with small vessel stroke (odds ratio [OR], 1.02 [95% CI, 0.95-1.10]), magnetic resonance imaging-confirmed lacunar stroke (OR, 0.95, [95% CI, 0.81-1.11]), nonlobar intracerebral hemorrhage (OR, 1.04 [95% CI, 0.72-1.50]), or vascular dementia (OR, 1.09 [95% CI, 0.95-1.25]). 5 key findings →

Evidence: low

Neighborhood deprivation was associated with poorer cognition (r = 0.36, p < 0.001), greater prevalence of modifiable risk factors (r = 0.36, p < 0.001), and greater SVD burden (β = 0.18, p = 0.008). 4 key findings →

Evidence: low

Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →

Evidence: low

1. Neuropsychological assessments indicated that the CSVD group scored significantly lower than the HC group in general cognitive level, memory, visuospatial ability, executive function, and language function (p < 0.05). 2. 5 key findings →

Participants: 40 Evidence: moderate

From across this tag

8 of the 903 studies in this tag, 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 8. The same 8 appear here every time.

↑ 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. 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