Question

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microscopic examinations of brain tissue reveal senile plaques (aggregations of beta - amyloid peptide) littering the brain like shrapnel between the neurons. it has been frustratingly difficult for researchers to uncover how beta - amyloid peptide acts as a (1 ), particularly because it is also present in healthy brain cells (but there is less of it). just what tips things off balance to favor production of more (2 ) is not understood, but it is known that this tiny peptide does its damage by enhancing calcium entry into certain brain neurons. high calcium levels can play a role in initiating apoptosis, or programmed cell death.
another line of research has implicated a (3 ) called tau, which appears to bind microtubule “tracks” together, much like railroad ties. in the brains of ad victims, tau grabs onto other tau molecules, forming spaghetti - like neurofibrillary tangles within neuron cell bodies. these (4 ) changes develop over several years, during which time family members watch the person they love “disappear”. it is a long and painful process. it is hoped that the lines of investigation, particularly stem cell research, will eventually merge and point to a treatment, but at present drugs that ease symptoms by (5 ) ach breakdown are most useful.

1. degenerative 2. inhibiting 3. neurotoxin 4. beta - amyloid 5. protein

1. protein 2. degenerative 3. inhibiting 4. neurotoxin 5. beta - amyloid

1. inhibiting 2. neurotoxin 3. beta - amyloid 4. protein 5. degenerative

1. neurotoxin 2. beta - amyloid 3. protein 4. degenerative 5. inhibiting

1. beta - amyloid 2. protein 3. degenerative 4. inhibiting 5. neurotoxin

Explanation:

Beta - amyloid peptide can act as a neurotoxin (1), more of it is not well - understood (2), tau is a protein (3), the changes are degenerative (4), and drugs that ease symptoms work by inhibiting ACh breakdown (5).

Answer:

1. neurotoxin 2. beta - amyloid 3. protein 4. degenerative 5. inhibiting