Provocative new research from Japan indicates that clumps of dysfunctional proteins, which can cause Alzheimer's and Creutzfeld-Jakob disease, can be passed from mother to offspring via the womb and also from mother's milk. The study on the spread of senile amyloidosis from affected mice to their nursing offspring was published in The American Journal of Pathology. One of the culprits that causes Alzheimer's is known as amyloidosis. Amyloidosis occurs when cellular proteins that normally float freely in the body form organized, nonfunctional clumps, or fibrils, that cause cellular damage. Depending on the protein involved, amyloidosis can lead to disorders such as Alzheimer's disease and Creutzfeld-Jakob disease.
While genetics are known to be involved in these disorders, the new study looked at whether the dysfunctional proteins could be passed directly to the pups born to affected mothers. Using mice that carry a mutation for senile amyloidosis, Dr. Xiaoying Fu injected female mice with amyloid fibrils, to accelerate their disease, and then allowed the mice to mate and produce offspring. The mouse pups born to these mothers exhibited elevated levels of amyloid fibrils that increased with age.
Interestingly, when mice born to injected mothers were nursed by control mothers (no fibrils injected), only one of nine pups had amyloid fibrils at 6 months. However, pups born to control mothers but nursed by injected mothers had amyloidosis at levels similar to that of pups born/nursed by injected mothers. The presence of fibrils in the milk of injected mothers was confirmed by protein assay and electron microscopy.
The researchers say that the ingestion of fibrils by nursing mouse pups - and not by events occurring in utero - transmits amyloid fibrils to their offspring, thus accelerating amyloidosis. Prion diseases, such as mad cow disease are known to be transmissible, but non-prion amyloidosis, however, had not been shown to spread in such a way until now. The implications could be far reaching and the researchers involved hope that their findings will trigger additional studies into amyloidosis.
Source: American Journal of Pathology
