**6. Conclusion**

The consumption of diets rich in cholesterol, fat, as well as another components (carbohy‐ drates) of the so called "Western diet" can contribute to increase the production of the peptide Aβ. This could contribute to brain amyloidosis by means of alteration of the selective perme‐ ability of the BBB, since BBB alterations are induced for these type of diets. In addition, it has been shown in the brain of transgenic animals that the amyloidosis can be accelerated by the intake of fat or cholesterol, which can lead to accumulation of Aβ in the brain. Besides that, the intake of fat or cholesterol can induce alterations in brain morphology and plasticity accompanied by a detrimental in cognitive abilities in animal models that resemble those alterations in cognitive abilities reported in AD patients, such as short-term memory, working memory, and learning flexibility. These evidences strongly suggest an association with the dietary habits and the possible development of AD in both cases, Early Onset Alzheimer's Disease or Late Onset Alzheimer's Disease, and a connection with systemic disruptions and brain functions **(Figure 5)**.

**Figure 5.** Diets rich on fat or cholesterol that are widely consume in Western countries can lead to develop dementia onset for several ways. One is the overproduction of systemic A*β* that can reach the brain due the chronic consume of these food components can affect the selective permeability of BBB. It can facilitate the pass of systemic A*β* as well as another molecules producing brain inflammation and A*β* deposits. It is accompanied for alterations in hippocampal plasticity and its cytoarchitecture. That can have an impact on brain functionality observed as memory failures. All these together can contribute to the development of dementia.
