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.

Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Highest usefulness score first. Studies without a score come last.

  1. PLD3 affects axonal spheroids and network defects in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature 2022-11-30 Digital health tools

    The precise mechanisms that lead to cognitive decline in Alzheimer's disease are unknown.

  2. TREM2 Gene Compound Heterozygosity in Neurodegenerative Disorders

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Journal of Alzheimer's disease : JAD 2022 TREM2 and immune genetics

    We identified a novel mutation c.401_406delinsTCTAT; p.(Asp134Valfs*55) in exon 3 of TREM2 in an Alzheimer's disease patient also carrying the p.Arg62His TREM2 variant.

  3. Tau-Centric Targets and Drugs in Clinical Development for the Treatment of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. BioMed research international 2016-06-26 Drug development

    The failure of several Phase II/III clinical trials in Alzheimer's disease (AD) with drugs targeting β-amyloid accumulation in the brain fuelled an increasing interest in alternative treatments against tau pathology, including approaches targeting tau phosphatases/kinases, active and passive immunization, and anti-tau aggregation.

  4. Transferrin receptor-targeted anti-amyloid antibody enhances brain delivery and mitigates ARIA

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Science (New York, N.Y.) 2025-08-07 Treatments

    Amyloid-related imaging abnormalities (ARIA), side effects of anti-amyloid drugs seen in magnetic resonance imaging of the brain, are a major safety concern in patients with Alzheimer's disease.

  5. Faulty autolysosome acidification in Alzheimer's disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature neuroscience 2022-06-02 Risk genes beyond APOE

    Autophagy is markedly impaired in Alzheimer's disease (AD).

  6. Molecular characterization of selectively vulnerable neurons in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature neuroscience 2021-01-11 Genetics

    Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown.

  7. Role of phosphodiesterases in the pathophysiology of neurodevelopmental disorders

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular psychiatry 2021-01-07 Down syndrome and Alzheimer's

    Phosphodiesterases (PDEs) are enzymes involved in the homeostasis of both cAMP and cGMP.

  8. TFEB regulates lysosomal exocytosis of tau and its loss of function exacerbates tau pathology and spreading

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular psychiatry 2020-05-04 Drug development

    Neurofibrillary tangles (NFTs) composed of hyperphosphorylated and misfolded tau protein are a pathological hallmark of Alzheimer's disease and other tauopathy conditions.

  9. Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature 2017-12-06 Disease mechanisms

    Alzheimer's disease is a common and devastating disease characterized by aggregation of the amyloid-β peptide.

  10. Preclinical and Clinical Development of ABBV-8E12, a Humanized Anti-Tau Antibody, for Treatment of Alzheimer's Disease and Other Tauopathies

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The journal of prevention of Alzheimer's disease 2017-01-01 Drug development

    Tau neurofibrillary tangles are found in the brains of patients suffering from Alzheimer's disease and other tauopathies.

  11. CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature communications 2016-04-15 Genetics

    Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping, fatal neurodegenerative disorders in which the molecular and pathogenic basis remains poorly understood.

  12. A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature medicine 2005-04-24 Cognitive tests and assessment

    Cholinergic neuron loss is a cardinal feature of Alzheimer disease.

  13. RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of Neuroscience 1999-03-15 Disease mechanisms

    In this study we used an in situ approach to identify the oxidized nucleosides 8-hydroxydeoxyguanosine (8OHdG) and 8-hydroxyguanosine (8OHG), markers of oxidative damage to DNA and RNA, respectively, in cases of Alzheimer's disease (AD).

  14. Increased poly(ADP-ribosyl)ation of nuclear proteins in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain : a journal of neurology 1999-02-01 Biomarkers

    Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+.

  15. Lewy Bodies Contain Altered α-Synuclein in Brains of Many Familial Alzheimer's Disease Patients with Mutations in Presenilin and Amyloid Precursor Protein Genes

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. American Journal Of Pathology 1998-11-01 Brain tissue and pathology

    Missense mutations in the alpha-synuclein gene cause familial Parkinson's disease (PD), and alpha-synuclein is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease (AD).

  16. Argyrophilic grain disease: widespread hyperphosphorylation of tau protein in limbic neurons

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Acta neuropathologica 1997-05-01 Drug development

    Argyrophilic grains (ArG) and coiled bodies of argyrophilic grain disease (AgD) and the neurofibrillary lesions of Alzheimer's disease (AD) share similar antigenic determinants, among them hyperphosphorylated microtubule-associated protein tau.

  17. Early-onset Alzheimer's disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Nature 1991-10-01 Risk genes beyond APOE

    A mutation at codon 717 of the beta-amyloid precursor protein gene has been found to cosegregate with familial Alzheimer's disease in a single family.

  18. Early proteasome downregulation and dysfunction drive proteostasis failure in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Brain : a journal of neurology 2025-12-04 Disease mechanisms

    Here, we integrated multiple approaches to characterize proteasome function, composition and regulation in post-mortem human AD brain tissue compared with age-matched controls.

  19. PolyGR-containing aggregates link with pathology and clinical features of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 2025-11-08 Brain tissue and pathology

    Alzheimer's disease is the most common form of dementia; however, its molecular mechanisms are not fully understood.

  20. Co-infection with two α-synuclein strains reveals novel synergistic interactions

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 2025-11-08 Brain tissue and pathology

    In synucleinopathies, the protein α-synuclein misfolds into Lewy bodies (LBs) in patients with Lewy body disease (LBD) or into glial cytoplasmic inclusions (GCIs) in patients with multiple system atrophy (MSA).

  21. LRRK2 kinase-mediated accumulation of lysosome-associated phospho-Rabs in tauopathies and synucleinopathies

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 2025-10-23 Brain tissue and pathology

    Parkinson's disease (PD) pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2) are associated with endolysosomal dysfunction across cell types, and carriers of LRRK2 mutations variably present with phosphorylated tau and α-synuclein deposits in post-mortem analysis.

  22. Genetic and proteomic analysis identifies BAG3 as an amyloid-responsive regulator of neuronal proteostasis

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 2025-10-14 Disease mechanisms

    The autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS) are the primary protein degradative mechanisms maintaining proteostasis in neurons.

  23. Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-10 Disease mechanisms

    We discovered that dendritic spine elimination-induced either artificially or in Aβ models-triggers a two-stage compensatory response: rapid enlargement of remaining spines followed by delayed spine regeneration.

  24. PINK1 deficiency permits the development of Lewy body dementia with coexisting Aβ pathology

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-09 Brain tissue and pathology

    DLB brains show PINK1 deficiency alongside α-syn and Aβ co-pathology.

  25. Mitochondrial DNA affects tau phosphorylation in aging and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-07 Biomarkers

    Relative to cybrids expressing mtDNA from CH individuals, MCI and AD cybrids contained more phosphorylated tau-217 (p-tau217), p-tau181, and total tau.

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