Neurodegenerative Disorders

Despite a diverse array of clinical manifestations and affected genes, many of the common neurodegenerative disorders share a similar molecular mechanism. Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS) and prion disease are each characterized by the aggregation of mutated or misfolded proteins into amyloid inclusion bodies. Aggregation results when the accumulation of misfolded proteins exceeds the cell's ability to eliminate them via the ubiquitin-proteasome degradation pathway. Some evidence suggests that these inclusions may represent a cellular defense mechanism intended to sequester toxic oligomers or to induce autophagic elimination of the diseased proteins. Effective future strategies for treatment of these neurodegenerative disorders rely on the understanding of the basic pathways affected in these disorders.

Disease	Type of Aggregation	Subcellular	Affected Protein	Brain Region Affected
Alzheimer's Disease (AD)	Neuritic Plaques	Extracellular	Amyloid beta peptide	Cortex, hippocampus, basal forebrain, brain stem
Alzheimer's Disease (AD)	Neurofibrillary tangles	Intracellular	Hyperphosphorylated Tau	Cortex, hippocampus, basal forebrain, brain stem
Parkinson's Disease (PD)	Lewy Body	Intracellular (Cytoplasm)	α-Synuclein	Substantia nigra, cortex, locus ceruleus, rephe (dopaminergic neurons)
Huntington's Disease (HD)	Intranuclear inclusions & cytoplasmic aggregates	Intracellular	Huntingtin with polyglutamate expansion	Striatum, basal ganglia, cortex, others
Amyotrophic Lateral Sclerosis (ALS)	Bonina bodies and axonal spheroids	Intracellular (Cytoplasm)	Various ALS genes	Spinal motor neurons and motor cortex
Prion Disease	Amyloid Plaque	Intracellular & Extracellular	Prion protein	Cortex, brain stem, thalamus, cerebellum, other

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