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. The Amyloid Cascade Hypothesis in Alzheimer's Disease: It's Time to Change Our Mind

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Current neuropharmacology 2017-01-01 Treatments

    Since its discovery in 1984, the beta amyloid peptide has treaded the boards of neurosciences as the star molecule in Alzheimer's disease pathogenesis.

  2. Oxidative Stress, Synaptic Dysfunction, and Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2017-01-01 Disease mechanisms

    Alzheimer's disease (AD) is a devastating neurodegenerative disorder without a cure.

  3. Analysis of 138 pathogenic mutations in presenilin-1 on the in vitro production of Aβ42 and Aβ40 peptides by γ-secretase

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2016-12-05 Biomarkers

    A hallmark of Alzheimer's disease (AD) is the aggregation of β-amyloid peptides (Aβ) into amyloid plaques in patient brain.

  4. Imaging synaptic density in the living human brain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science translational medicine 2016-07-01 Disease mechanisms

    Chemical synapses are the predominant neuron-to-neuron contact in the central nervous system.

  5. In addition to a prominent role in glycemic control, glucagon-like peptide 1 (GLP-1) receptor agonists exhibit neuroprotective properties.

  6. NEURODEGENERATION. Alzheimer's and Parkinson's diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2015-08-01 Brain tissue and pathology

    The pathological assembly of Aβ, tau, and α-synuclein is at the heart of Alzheimer's and Parkinson's diseases.

  7. α-Synuclein strains cause distinct synucleinopathies after local and systemic administration

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2015-06-10 Vascular contributions

    Misfolded protein aggregates represent a continuum with overlapping features in neurodegenerative diseases, but differences in protein components and affected brain regions.

  8. Patterns of Tau and α-Synuclein Pathology in the Visual System

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Parkinson's disease 2015 Brain tissue and pathology

    We detected immunoreactivity for all proteins along the optic pathway.

  9. GABA from reactive astrocytes impairs memory in mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2014-06-29 Inflammation and the immune system

    In Alzheimer's disease (AD), memory impairment is the most prominent feature that afflicts patients and their families.

  10. The role of autophagy in neurodegenerative disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2013-08-06 Disease mechanisms

    Autophagy is a lysosomal degradative process used to recycle obsolete cellular constituents and eliminate damaged organelles and protein aggregates.

  11. Tau deficiency induces parkinsonism with dementia by impairing APP-mediated iron export

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2012-01-29 Brain scans and imaging

    The microtubule-associated protein tau has risk alleles for both Alzheimer's disease and Parkinson's disease and mutations that cause brain degenerative diseases termed tauopathies.

  12. Molecular chaperones in protein folding and proteostasis

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2011-07-20 Disease mechanisms

    Most proteins must fold into defined three-dimensional structures to gain functional activity.

  13. Neural mechanisms of ageing and cognitive decline

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2010-03-01 How common it is

    During the past century, treatments for the diseases of youth and middle age have helped raise life expectancy significantly.

  14. Functional amyloids as natural storage of peptide hormones in pituitary secretory granules

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2009-06-18 Risk factors

    Amyloids are highly organized cross-beta-sheet-rich protein or peptide aggregates that are associated with pathological conditions including Alzheimer's disease and type II diabetes.

  15. Lithium Trial in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of Clinical Psychiatry 2009-06-15 Drug development

    No treatment effect on GSK-3 activity or CSF-based biomarker concentrations (P >. 05) was observed.

  16. S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2009-04-01 Disease mechanisms

    Mitochondria continuously undergo two opposing processes, fission and fusion.

  17. Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2008-09-21 Disease mechanisms

    Cyclophilin D (CypD, encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose opening leads to cell death.

  18. Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of beta-secretase

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2008-06-29 Risk genes beyond APOE

    Recent efforts have revealed that numerous protein-coding messenger RNAs have natural antisense transcript partners, most of which seem to be noncoding RNAs.

  19. Recovery of learning and memory is associated with chromatin remodelling

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2007-04-29 Brain scans and imaging

    Neurodegenerative diseases of the central nervous system are often associated with impaired learning and memory, eventually leading to dementia.

  20. Atomic structures of amyloid cross-beta spines reveal varied steric zippers

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2007-04-29 Brain tissue and pathology

    Amyloid fibrils formed from different proteins, each associated with a particular disease, contain a common cross-beta spine.

  21. Control of peripheral nerve myelination by the beta-secretase BACE1

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2006-09-21 Risk genes beyond APOE

    Although BACE1 (beta-site amyloid precursor protein-cleaving enzyme 1) is essential for the generation of amyloid-b peptide in Alzheimer's disease, its physiological function is unclear.

  22. Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2006-09-01 Risk genes beyond APOE

    Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo.

  23. S-nitrosylated protein-disulphide isomerase links protein misfolding to neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2006-05-01 Disease mechanisms

    Stress proteins located in the cytosol or endoplasmic reticulum (ER) maintain cell homeostasis and afford tolerance to severe insults.

  24. The importance of sequence diversity in the aggregation and evolution of proteins

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2005-12-01 Prevention trials

    Incorrect folding of proteins, leading to aggregation and amyloid formation, is associated with a group of highly debilitating medical conditions including Alzheimer's disease and late-onset diabetes.

  25. Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2005-06-01 Disease mechanisms

    The self-renewing epithelium of the small intestine is ordered into stem/progenitor crypt compartments and differentiated villus compartments.

From across this topic

9 of the 1,352 studies in this topic, 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 9. The same 9 appear here every time.

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