Abstract: Classical hallmarks of Alzheimer's disease (AD) are a synaptic loss, cholinergic neuron death, and
abnormal protein deposition, particularly of toxic amyloid - β peptide (Aβ) that is derived from amyloid - β protein precursor (AβPP) by the action of beta - and gamma - secretases.
Classical hallmarks of Alzheimer's disease (AD) are a synaptic loss, cholinergic neuron death, and
abnormal protein deposition, particularly of toxic amyloid - β peptide (Aβ) that is derived from amyloid - β protein precursor (AβPP) by the action of beta - and gamma - secretases.
The ability of colchicine to interfere with this sort of structural protein formation has led to its use in
abnormal protein depositions such as amyloidosis.
Not exact matches
«We still do not understand fully how these
abnormal amyloid and tau
protein depositions affect brain functions and cause dementia,» stated Satoshi Minoshima, MD, PhD, chair of the SNMMI Scientific Program Committee.