[6] Sacks and Paul Alan Cox subsequently wrote that bats had been feeding on Federico nuts (Cycas micronesica) and concentrating β-methylamino-L-alanine (BMAA), a known neurotoxin, in their body fat.
[citation needed] Patient presentations include muscle atrophy, maxillofacial paralysis, inability to speak or swallow and subsequent choking.
[citation needed] Diaphragm and respiratory accessory muscles can become paralyzed, necessitating mechanical ventilation to facilitate breathing.
[citation needed] No standard form of bodig has been reported and the documented cases of the disease manifested in many different clinical presentations.
Those who experience dementia are often aphasic and restless, and demonstrate irrational behavior, such as violence, and deep emotions at odd intervals.
Except in cases with concurrent dementia, most patients are capable of lucid thought and speech throughout the disease's physical progression.
[citation needed] Some hypotheses as to the cause of the disease include genetics, cycad seeds, and ingested beta-Methylamino-L-alanine (BMAA) from the consumption of fruit bats.
[11] Targeted high-throughput sequencing in a relatively small sample demonstrates that disease in many patients can be explained by pathogenic mutations in known genes for neurodegeneration.
Not only that, after nearly two decades of NIH-funded research, animal models failed to reproduce chronic Lytico-Bodig, and the hypothesis was rejected for the first time.
[5] In 1967, following studies that linked lathyrism to ODAP, Marjorie Whiting, a nutritional anthropologist, asked Arthur Bell, a plant biochemist, to test cycad seeds for their chemical constituents.
[16] The cycad hypothesis was resurrected by Paul Alan Cox and Oliver Sacks, after re-examining aspects of the Chamorro diet.
[10][18] Support for the BMAA theory of the Guam disease came from the finding reported in 2016 that chronic dietary exposure of vervet monkeys homozygous for the APOE4 gene (which in humans increases risk of Alzheimer's disease) to the cyanobacterial toxin BMAA produces dense neurofibrillary tangles and sparse amyloid plaques similar to that found in the brains of Chamorro villagers in Guam who died from lytico-bodig.
Shifting to a higher power, he saw a huge number of neurofibrillary tangles, densely staining, convoluted masses, harshly evident within the destroyed nerve cells.
It seems in the case of the Chamorros, family members are the primary caregivers, and they have accepted those who are ill and provide home care for all those inflicted with lytico-bodig.