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๐Ÿ“ฐ Latest breakthroughs
๐Ÿ—บ๏ธ Disease Atlas ยท Psychiatric disorder

late-onset Alzheimers disease

This is the most common form of the disease, which happens to people age 65 and older. It may or may not run in families. So far, researchers havenโ€™t found a particular gene that causes it. No one knows for sure why some people get it and others donโ€™t.

๐Ÿ”” Follow weekly
๐Ÿงฌ229genes / proteins with evidence
๐Ÿ’Š0drugs and clinical candidates
๐Ÿงช8recruiting trials worldwide
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Understand late-onset Alzheimers disease

Brain and nerves ยท Nerve cells that slowly stop working
๐ŸŽ“ Learn more

What it is

Alzheimer's disease (AD) is the most common form of dementia among older people. Dementia is a brain disorder that seriously affects thinking and memory skills. If you have AD, it can impair your ability to reason or learn new skills until it becomes difficult to complete daily activities.

AD begins slowly over many years. It first involves the parts of the brain that control thought, memory, and language. It may be mistaken for normal memory changes with aging. However, AD is not a normal part of aging. The brain changes from the disease lead to symptoms that get worse over time.

What are the symptoms of Alzheimer's disease?

From MedlinePlus: Alzheimer's Disease (US National Library of Medicine) โ†—

๐Ÿง  Brain and nerves: In neurodegenerative diseases, nerve cells in the brain or spinal cord stop working and die over time - affecting memory (Alzheimer's disease), movement (Parkinson's disease) or muscles (ALS).

โ“ Why it happens

  • Proteins fold the wrong way and clump together inside or between nerve cells - amyloid and tau in Alzheimer's disease, alpha-synuclein in Parkinson's disease.
  • Inflammation, some genes (such as APOE4) and, above all, age raise the risk.

๐Ÿซ€ What it does to the body

  • As connections between nerve cells are lost, memory, thinking, movement or speech fade.
  • The changes start years - often decades - before the first symptoms.

๐Ÿงฑ Why it is hard to cure

  • Most medicines cannot easily pass the blood-brain barrier that protects the brain.
  • By the time symptoms appear, many nerve cells are already lost, and they do not grow back.
  • Many drug trials have failed, partly because the diseases are found late.

๐Ÿš€ What research is trying now

  • Antibodies that clear amyloid and modestly slow early Alzheimer's disease (approved in some countries).
  • Blood tests that detect Alzheimer's changes years earlier.
  • Gene-targeted medicines, such as one approved in the US for an inherited form of ALS.

General information about brain and nerves, reviewed by people; it does not describe any one person. Below: the evidence for late-onset Alzheimers disease itself.

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AI briefing

Where the science on late-onset Alzheimers disease stands, from the evidence on this page

AI reads the targets, drugs, trials and papers below and writes where the science stands โ€” every claim cited. It is shared with everyone who opens late-onset Alzheimers disease.

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Top targets

Genes and proteins ranked by Open Targets evidence (0-1)
APOE apolipoprotein EPROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.64
CR1 complement C3b/C4b receptor 1 (Knops blood group)PROTACantibodyother๐ŸงŠ AlphaFold structure โ†— 0.46
CLU clusterinPROTACantibody๐ŸงŠ AlphaFold structure โ†— 0.41
APP amyloid beta precursor proteinPROTACantibodyothersmall molecule๐ŸงŠ AlphaFold structure โ†— 0.40
ABI3 ABI family member 3PROTAC๐ŸงŠ AlphaFold structure โ†— 0.36
GRN granulin precursorPROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.36
ATP5F1C ATP synthase F1 subunit gammaPROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.35
APH1B aph-1B gamma-secretase subunitPROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.34
ACE angiotensin I converting enzymePROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.34
BIN1 bridging integrator 1PROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.34
ADAM10 ADAM metallopeptidase domain 10PROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.33
PLCG2 phospholipase C gamma 2PROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.33
TREM2 triggering receptor expressed on myeloid cells 2antibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.33
SORL1 sortilin related receptor 1PROTACantibody๐ŸงŠ AlphaFold structure โ†— 0.33
CD33 CD33 moleculePROTACantibodyothersmall molecule๐ŸงŠ AlphaFold structure โ†— 0.32

Green labels: what the target is known to be druggable by. The score combines genetics, somatic mutations, drugs, expression and literature.

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Drugs and candidates

Every medicine linked to late-onset Alzheimers disease, by how far it has got

No drugs recorded yet.

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AI Cure shows public evidence (Open Targets, ClinicalTrials.gov, PubMed, openFDA, DepMap, AlphaFold) with its source, and AI summaries that cite it โ€” not medical advice and not a cure. Treatment decisions belong with your doctor. Research ideas are shared only with approved researchers and labs, who can test them. In an emergency call your local emergency number (112 in India and Europe, 911 in the US). AI Cure Terms of Use ยท Privacy