The single-mutation of genes associated with Alzheimer's disease (AD) increases the production of A beta peptides. An elevated concentration of A beta peptides is prone to aggregation into oligomers and further deposition as plaque. A beta plaques and neurofibrillary tangles are two hallmarks of AD. In this review, we provide a broad overview of the diverses sources that could lead to AD, which include genetic origins, A beta peptides and tau protein. We shall discuss on tau protein and tau accumulation, which result in neurofibrillary tangles. We detail the mechanisms of A beta aggregation, fibril formation and its polymorphism. We then show the possible links between A beta and tau pathology. Furthermore, we summarize the structural data of A beta and its precursor protein obtained via Nuclear Magnetic Resonance (NMR) or X-ray crystallography. At the end, we go through the C-terminal and N-terminal truncated A beta variants. We wish to draw reader's attention to two predominant and toxic A beta species, namely A beta(4-42) and pyroglutamate amyloid-beta peptides, which have been neglected for more than a decade and may be crucial in A beta pathogenesis due to their dominant presence in the AD brain.