Familial Alzheimer’s Disease
- Age-Related Macular Degeneration
- Alzheimer’s Disease
- Amyotrophic Lateral Sclerosis
- Autism Spectrum Disorder
- Chronic Mental Diseases
- Chronic Traumatic Encephalopathy
- Conjunctival Amyloidosis
- Corticobasal Degeneration
- Creutzfeldt–Jakob Disease
- Dementia With Lewy Bodies
- Dentatombral-Pallidoluysian Atrophy
- Desmin-Related Cardiomyopathy
- Dialysis-Related Amyloidosis
- Familial Alzheimer’s Disease
- Familial Amyloidotic Cardiomyopathy
- Familial Amyloidotic Polyneuropathy
- Familial Amyotrophic Lateral Sclerosis
- Familial British Dementia
- Familial Danish Dementia
- Familial Fatal Insomnia
- Familial Mediterranean Fever
- Familial Oculoleptomeningel Amyloidosis
- Familial Parkinson’s Disease
- Finnish Hereditary Systemic Amyloidosis
- Frontotemporal Dementia
- Gerstmann–Sträussler–Scheinker Syndrome
- HIV Infection
- Hereditary Cerebral Amyloid Angiopathy
- Hereditary Non-Neuropathic Systemic Amyloidosis
- Hereditary Renal Amyloidosis
- Huntington’s Disease
- Inclusion Body Myositis
- Insulin-Related Amyloidosis
- Isolated Atrial Amyloidosis
- Medullary Carcinoma Of The Thyroid
- Multiple Systems Atrophy
- Parkinson’s Disease
- Pick’s Disease
- Preeclampsia
- Primary Amyloidosis
- Progressive Supranuclear Palsy
- Prostatic Amyloidosis
- Pure Autonomic Failure
- Senile Systemic Amyloidosis
- Spinal And Bulbar Muscular Atrophy
- Spinal Cord Injury And Traumatic Brain Injury
- Spinocerebellar Ataxia Types 1, 2, 3, 6, 7, And 17
- Systemic (Reactive) Aa Amyloidosis
- Type-2 Diabetes Mellitus
(FAD) is very rare; less than 1% of AD patients have FAD. FAD Patients with FAD become sick at a relatively young age, typically, in their 40s or 50s, and the disease is more aggressive than sporadic AD. FAD can be caused by mutations in three different genes. The most common ones are in presenilin 1, which is involved in the production of amyloid β-protein (Aβ). Mutations in a counterpart gene called presenilin 2 have a similar impact. Both cause an increase in production of more toxic forms of Aβ. The third gene is the one producing the amyloid β-protein precursor itself, from which Aβ is produced. These mutations cause elevated production of Aβ or of Aβ forms that are more toxic and more prone to aggregation.